The Janus kinase 2 (JAK2) V617F mutation is recognized as a defining molecular lesion in Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs). This mutation was recognized in the context of clonal hematopoiesis of indeterminate potential, which has recently been linked with cardiovascular disease. Recent evidence has demonstrated a significant correlation between JAK2 mutations and thoracic aortic aneurysm (TAA) a condition frequently lacking identifiable risk factors. A scoping review, involving MEDLINE, Embase, Web of Science, Google Scholar, and prominent hematology and cardiology conference abstracts (from inception to August 2025) was performed. All studies that indicate a correlation between JAK2 mutations and aortic aneurysms were included. Seven studies with a total of 446,839 participants were found. Among these, 745 (0.17%) tested positive for JAK2. Data consistently indicated an elevated risk of thoracic aortic aneurysm (TAA), but not abdominal aortic aneurysm, in individuals with JAK2 mutations. Proposed mechanisms include inflammatory cytokine signaling, macrophage activation, and degradation of the extracellular matrix. Emerging clinical data indicate a consistent association between JAK2 V617F-mutated clonal hematopoiesis or myeloproliferative neoplasms and thoracic aortic aneurysm, with less consistent findings for abdominal aneurysm. Although experimental studies suggest that JAK2-driven inflammatory signaling and extracellular matrix remodeling may contribute to vascular wall injury, these mechanisms remain largely inferential and do not establish causality. Well-designed prospective investigations incorporating standardized imaging, uniform aneurysm definitions, and stratification by clonal burden and disease context will be necessary to better define risk and determine whether JAK2-associated clonal hematopoiesis has implications for vascular surveillance or prevention strategies.

Modern knowledge about the principles of clonal hematopoiesis of indeterminate potential (CHIP) has paved way for numerous clinical efforts aimed at managing this pre-malignant condition. The emergence of various CHIP clinics across the globe attests to collaborative attempts to formalize clinical management of CHIP and its entities. However, translational science in this field is limited to date, partly due to nascent therapeutic concepts with limited understanding of natural history and longitudinal follow up. Here, we explore the structure and function of existing CHIP clinics and propose a working model to materialize future CHIP clinics at academic and community health care systems. We discuss the critical elements in conceptualizing and operationalizing CHIP clinic workflows, including pinpointing unmet clinical needs, prospective and retrospective identification of patients with CHIP, and recruitment of key CHIP clinic personnel toward creation of an effective multidisciplinary team. We underscore the clinical utility of CHIP clinics with regard to value creation in preventive hematology, real-world risk assessment using evidence-based models, provision of clinical trial enrollment opportunities, establishment of curated research registries and tissue biorepositories, and development of community outreach efforts. Finally, we shed light onto prospects of continued multi-center participation in collaborative science related to emerging therapeutic options in CHIP. These concepts may have a favorable impact on previvorship in hematology in the coming years.

An exploratory study of environmental and nutritional determinants of early-stage clonal hematopoiesis in the elderly.

Abstract Background Patients with chronic kidney disease (CKD) exhibit an extremely high prevalence of coronary artery disease. Clonal hematopoiesis of indeterminate potential (CHIP) and CKD share pathological features such as aging, chronic inflammation, and accelerated atherosclerosis. Their coexistence can synergistically exacerbate vascular damage and increase coronary risk. However, the association between CHIP and specific coronary lesions in CKD populations has not been reported, and its relationship with cardiovascular events remains controversial. Methods A total of 151 patients with CKD who underwent coronary angiography were prospectively included. To evaluate the status of CHIP, we utilized high-depth targeted sequencing, and measured serum inflammatory factor levels. Furthermore, we systematically followed up these patients to document the occurrence of adverse clinical events. Results CHIP was identified in 65 (43.0%) CKD patients, with the carrier rate steadily rising with age. The CHIP subjects had higher rates of left circumflex (LCx) stenosis, three-vessel disease, and Gensini scores than non-CHIP patients (all P < 0.05). After adjusting for relevant clinical risk factors, the presence of CHIP continued to show an independent association with three-vessel disease (OR 2.26, 95% CI 1.07–4.75; P = 0.032). The survival analysis indicated that CHIP, along with non-DNMT3A mutations and a larger clone size (variant allele frequency ≥ 0.10), correlated with the primary composite endpoint (P < 0.01). Even after controlling for various clinical variables, the CHIP status still demonstrated an independent association with the primary composite endpoint (HR 2.02, 95% CI 1.11–3.67; P = 0.022). Conclusions CHIP was associated with the severity of coronary lesions and unfavorable clinical outcomes in patients with CKD.

A major scientific drive is to characterize the protein-coding genome, which is a primary basis for studying human health. But the fundamental question remains of what has been missed in previous analyses. Over the past decade, the translation of non-canonical open reading frames (ncORFs) has been observed across human cell types and disease states1-3, with major implications for biomedical science. However, a key gap in knowledge has been which ncORFs produce small microproteins or alternative protein molecules that contribute to the human proteome. Here we report the collaborative efforts of the TransCODE Consortium4 to produce a consensus landscape of protein-level evidence for ncORFs. We show that about 25% of a set of 7,264 ncORFs gives rise to detectable peptides in a large-scale analysis of 95,520 proteomics experiments. We develop an annotation framework for ncORF-encoded microproteins as human proteins and codify the new conceptual model of 'peptideins' as microproteins that have indeterminate potential as functional proteins. To probe the biological implications of peptideins, we create an evolutionary analysis approach, termed ORF relative branch length (ORBL), and determine that evolutionary constraint is common and associates with observation of ncORF-derived peptides. We then characterize a pan-essential cellular phenotype for one peptidein from the OLMALINC long non-coding RNA. Overall, we generate public research tools supported by GENCODE and PeptideAtlas and advance biomedical discovery for understudied components of the human proteome.

Aging is a complex biological process uniquely shaped in women by hormonal transitions, particularly across the menopause transition. While chronological age alone fails to capture individual health variability, emerging molecular biomarkers offer tools to quantify biological aging and understand mechanisms underlying age-related decline. This review synthesizes the current landscape of aging biomarkers, including senescence-associated secretory phenotype factors, epigenetic clocks, clonal hematopoiesis of indeterminate potential, and telomere length, with a particular emphasis on their relevance to menopause. This narrative review synthesizes human studies, translational research, and foundational basic science identified through PubMed searches through June 2025, examining aging biomarkers in general populations, among women in the menopause transition, and in relation to vasomotor symptoms and hormone therapy. Evidence demonstrates that changes in biological aging biomarkers are observed across multiple molecular systems during midlife, including the menopause transition, reflecting broader age-related biological remodeling. Postmenopausal status, particularly following early or surgical menopause, has been associated with biological aging phenotypes, including elevated senescence-associated secretory phenotype factors, epigenetic age acceleration, clonal hematopoiesis, and shorter leukocyte telomere length, likely reflecting a combination of chronological aging, hormonal changes, and individual biological vulnerability. While severe vasomotor symptoms have been linked to higher epigenetic age, hormone therapy may favorably influence certain senescence markers and biological age discrepancy. Despite these advances, significant limitations constrain clinical translation, as current biomarkers capture overlapping biological processes and lack validated thresholds to define biological aging, especially in women. Future research requires large, longitudinal studies across diverse populations to establish clinically meaningful thresholds and sex-specific calibration. Advancing precision health strategies for women requires a better understanding of how reproductive and hormonal factors modify biomarker trajectories to improve risk prediction and to facilitate the development of targeted interventions for age-related diseases.

It has been known that the cytokine TNF (tumor necrosis factor alpha) influences hematopoiesis for decades. We now know that increases in TNF in the aging microenvironment favor the persistence and expansion of myeloid progenitors, especially those that contain mutations associated with clonal hematopoiesis of indeterminate potential (CHIP). Herein, we will examine both seminal and recent studies that have advanced our understanding of how TNF shapes hematopoietic development during aging and influences clonal dynamics in CHIP. Elevated levels of TNF contribute to engraftment and expansion of CHIP-mutant clones; however, there are subtle differences between the specific CHIP mutations. Sex differences in levels of TNF may contribute to differences in the frequency and types of CHIP mutations found in males and females. Anti-TNF inhibitors reduce the frequency of CHIP mutation containing clones in multiple inflammatory diseases. The elevated levels of TNF that occur with both age and chronic inflammatory conditions contribute to both myeloid skewing and CHIP. Anti-TNF drugs reduce problematic changes in myeloid hematopoiesis. Anti-TNF drugs are not an effective strategy to treat CHIP and more research is needed as to whether other anti-inflammatory strategies, including diet and exercise, are also effective.

Immune-endothelial crosstalk in cardiovascular inflammation: Canakinumab at the intersection of mechanism and precision therapy.

Connecting the dots: Gouty arthritis, clonal haematopoiesis and myeloid activation, in a unified inflammation model for atherosclerosis progression.

Aplastic anemia (AA) results from T-cell-mediated destruction of hematopoietic stem and progenitor cells (HSPCs), driving clonal hematopoiesis via loss of human leukocyte antigen (HLA) risk alleles (HLA loss-of-function mutations or uniparental disomy 6p, UPD6p), paroxysmal nocturnal hemoglobinuria and clonal hematopoiesis of indeterminate potential (CHIP) mutations. Here genomic profiling of 619 patients with AA revealed clonal hematopoiesis in 69% of cases, with ASXL1, BCOR and BCORL1 identified as the most frequent CHIP mutations in pediatric cases. Single-cell multi-omics analysis of 304,902 cells from 48 samples uncovered complex branching clonal architecture, with a median of three HLA loss events per patient, converging to inactivate HLA risk alleles. Single-cell whole-genome sequencing (WGS) resolved up to 15 HLA loss clones per patient and phylogenetic reconstruction indicated that these clones originated years before diagnosis. Long-read WGS precisely mapped UPD6p breakpoints and HLA methylation. HLA loss conferred a protective effect against CHIP, evidenced by their near-absent co-occurrence. Longitudinal single-cell analysis demonstrated that long-lived clones were enriched in the CD34+ HSPC compartment. These findings reveal parallel evolutionary pathways used by hematopoietic cells to evade immune attack.

Clonal haematopoiesis is associated with protection against angina pectoris in the UK population.

Clonal hematopoiesis of indeterminate potential (CHIP) is an age-associated condition whose population-level characteristics and clinical concordance in Japan remain incompletely defined. We analyzed whole-genome sequencing data from 49,982 participants in the Tohoku Medical Megabank (TMM) cohort to characterize the prevalence, mutational spectrum, age dependency, and clinical relevance of CHIP. CHIP mutations were detected in 1234 individuals (2.5%), comprising 1413 variants across 1015 loci. DNMT3A and TET2 were the most frequently mutated genes, whereas ASXL1 and PPM1D mutations were less prevalent than reported in Western cohorts. Four recurrent CHIP candidate loci (ZNF318, SMC3, CBL, and GNAS) were identified, most of which were predicted to be oncogenic. Comparison with TOPMed and UK Biobank datasets demonstrated overall concordance in variant prevalence, with differences observed for selected driver mutations. dN/dS analysis indicated positive selection in the majority of CHIP-associated genes. Concordance with clonal hematopoiesis (CH) mutations detected in cancer patients was evaluated using data from the MONSTAR-SCREEN-2 study with paired leukocyte sequencing. When focusing on genes in which CHIP mutations have been reported, 66% were confirmed as CH, yielding a positive predictive value of 66% and a negative predictive value of 76%. CHIP prevalence increased significantly with age, exceeding 5% in individuals aged ≥ 70 years, with an estimated 3.4% increase per additional year of age. Higher variant allele frequency mutations showed a slightly stronger age association. These findings define the landscape of CHIP in the Japanese population and clarify its relationship to CH detected by cancer-focused liquid biopsy assays.

Only a minority of patients with advanced gastric cancer (GC) or esophagogastric junction (EGJ) adenocarcinoma derive durable benefit from anti-programmed cell death 1 (PD-1) therapy. However, reliable biomarkers for real-world clinical decision-making remain limited. To identify tumor site-specific genomic alterations associated with outcomes of nivolumab monotherapy in a nationwide real-world cohort. We conducted a retrospective nationwide analysis using Japan's Center for Cancer Genomics and Advanced Therapeutics (C-CAT) registry, including patients with GC and EGJ cancer adenocarcinoma treated with nivolumab monotherapy (July 2019-April 2024). Primary endpoints were time to treatment failure (TTF) and overall survival (OS), defined as the interval from nivolumab initiation to death from any cause; objective response rate (ORR) was secondary. Gene-level alteration indicators were derived from vendor-reported tumor-only panel calls across multiple platforms and filtered for clonal hematopoiesis of indeterminate potential (CHIP)-like variants (variant allele frequency < 0.05). Multivariable models adjusted for age and sex were fitted separately for GC and EGJ cancer. Variant pathogenicity was based on available panel annotations; therefore, gene-level results should be interpreted as exploratory findings. Among 798 patients with GC and 114 patients with EGJ cancer adenocarcinoma, median TTF/OS/ORR were 3.98 months/20.2 months/11.7% in GC and 4.80 months/24.7 months/14.9% in EGJ cancer adenocarcinoma. In GC, ASXL1 mutation remained independently associated with longer TTF (hazard ratio [HR] 0.59, 95% confidence interval [CI] 0.37-0.94) after adjustment and CHIP filtering. For OS, microsatellite instability-high [MSI-H] (HR 0.16, 95% CI 0.04-0.70) and FANCG (HR 0.37, 95% CI 0.16-0.87) were associated with longer OS, whereas CDH1 (HR 1.51, 95% CI 1.10-2.05) was associated with shorter OS. In EGJ cancer adenocarcinoma, NTRK1 mutation correlated with longer TTF (HR 0.31, 95% CI 0.10-0.98) and MUTYH with shorter OS (HR 5.68, 95% CI 2.04-15.81), both exploratory. In this large Japanese real-world cohort, genomic associations with nivolumab outcomes differed by tumor site. In gastric cancer, ASXL1 mutation was associated with prolonged treatment benefit under PD-1 blockade, while CDH1 and FANCG showed exploratory associations with OS. These findings warrant further validation in prospective and platform-controlled analyses.

Background Clonal hematopoiesis of indeterminate potential (CHIP)-associated somatic mutations are associated with increased cardiovascular and cerebrovascular risk in the general population; whether mutations detected at myeloid neoplasm (MN) diagnosis predict incident cardiovascular and cerebrovascular events (CCVEs) is unclear. Methods We retrospectively studied 203 adults with newly diagnosed myelodysplastic neoplasms, myelodysplastic/myeloproliferative neoplasms, or acute myeloid leukemia unfit for intensive chemotherapy (2016–2023) who underwent pretreatment next-generation sequencing. Cause-specific hazard models adjusted for cardiovascular risk factors assessed associations between CHIP-associated gene mutations and incident CCVEs, including age-stratified and age-by-mutation interaction analyses. Results Median age was 68 years (IQR, 61–75); 127 (62.6%) were male; 141 (69.5%) carried ≥1 CHIP-associated gene mutation, most commonly ASXL1, TET2, TP53, or DNMT3A. Over median 12-month follow-up, 74 (36.5%) experienced a first CCVE. Any CHIP-associated gene mutation was associated with CCVE risk in univariable analysis; this association was not significant after multivariable adjustment (adjusted hazard ratio [aHR], 1.58; 95% CI, 0.87–2.88; p=0.13). In joint age-mutation analyses, mutation-positive patients aged ≥70 years had the highest CCVE risk (aHR, 2.77; 95% CI, 1.17–6.56), whereas younger mutation-positive patients showed a nonsignificant trend (aHR, 2.16; 95% CI, 0.90–5.20; p=0.085); interaction was not significant (p=0.29). In multivariable models, CHIP-associated gene mutations, higher-risk MN, and incident CCVEs were each associated with higher all-cause mortality. Conclusions CHIP-associated gene mutations at MN diagnosis were not independently associated with incident CCVEs. Older mutation-positive patients had higher observed CCVE risk, predominantly heart failure, with limited precision. These exploratory findings warrant prospective multicenter validation.

Periodontitis is now recognized not merely as a localized oral condition but as a systemic disease linked to over 70 communicable and non-communicable conditions. This Review explores the key mechanistic pathways-or "gum-shots"-underpinning the systemic impact of periodontitis. Seven interwoven mechanisms are identified. The first, microbial translocation, involves oral pathobionts and virulence factors breaching anatomical barriers and gaining systemic access via hematological, respiratory, and enteral routes, contributing to tissue damage at extra-oral sites. The second, systemic (meta)inflammation, implicates both the spillover of inflammatory mediators from periodontal tissues into circulation and the immune response to translocated pathogens, fueling pro-inflammatory processes. The third, maladaptive myelopoiesis, involves the periodontitis-associated maladaptive trained immunity and aging-related clonal hematopoiesis of indeterminate potential in the bone marrow, leading to myeloid cells with heightened proinflammatory potential. The fourth, immune players trafficking, centers on the systemic repercussions of periodontally generated autoantibodies, translocated orally primed inflammatory cells, and other local immune events. The fifth, masticatory dysfunction-mediated dietary alterations, involves compromised chewing efficiency that alters dietary intake, resulting in nutritional and metabolic imbalances. The sixth, functional dysregulation of the oral microbiome, describes how periodontitis alters the metabolic activity of this densely populated microbial "superorganism", with downstream effects on both oral and systemic physiology. The final mechanism, shared underlying vulnerabilities, refers to background entities-such as biological aging, oxidative stress, psychosocial stress, (epi)genetic predispositions, certain viral infections, and potentially other as-yet-unknown contributors-that drive multi-morbidity, including periodontitis. By dissecting these interconnected pathways, this critical Review challenges the traditional dichotomy of direct versus indirect mechanisms, revealing a more intricate and dynamic interplay.

Clonal hematopoiesis of indeterminate potential (CHIP) is the clonal expansion of somatically mutated hematopoietic stem cells (HSCs) in the bone marrow. CHIP mutations are relatively common in multiple myeloma (MM) and have been identified as potential biomarkers for poorer survival outcomes. MM is a hematological malignancy that, despite treatment advances, remains aggressive and incurable for many patients. The potential impact of CHIP mutations on the outcomes of MM treatments has been the topic of several recent studies, yet both the magnitude and the modality by which CHIP exerts its negative effects on treatment and disease progression remain to be fully elucidated. Evidence suggests that CHIP mutations may contribute to inferior survival and treatment tolerances, as well as contribute to greater treatment toxicity and related frailty. In this review, we synthesize and discuss the available literature to provide an updated understanding of the complex role that CHIP plays in altering the MM microenvironment, and the resulting impact on standard MM treatments, autologous stem cell transplant (ASCT) and B-cell maturation antigen (BCMA)-targeted therapy/CAR-T, and the important role of immunomodulatory drug (IMiD) maintenance therapy in clinical outcomes.

Rationale:Sepsis is a life-threatening syndrome causing significant morbidity and mortality especially in the aging population. Clonal hematopoiesis of indeterminate potential (CHIP) is an age-related condition of clonal expansion of hematopoietic stem cells harboring somatic mutations associated with increased incidence of chronic illness and all-cause mortality.Objective:Evaluate the association of pre-illness CHIP with mortality and morbidity in patients admitted to the ICU with sepsis.Methods:We performed a retrospective study using a de-identified electronic health record linked with a DNA biorepository. We identified adult patients with sepsis who had DNA collected prior to ICU admission. We tested the association between CHIP status, determined from whole-genome sequencing, and ICU mortality, organ support-free days, and long-term survival adjusting for age, sex, race and Sequential Organ Failure Assessment (SOFA) score on ICU admission.Measurements and Main Results:Pre-illness CHIP was associated with increased sepsis mortality (OR = 1.54, 95% CI 1.13 to 2.07, P = 0.005) and fewer days alive and free of organ support (−1.7 days, 95% CI −3.2 to −0.2, P = 0.028) after adjusting for age, sex, race, and SOFA score. In sepsis survivors, CHIP was also associated with increased long-term mortality after discharge (HR 1.40, 95% CI 1.01 to 1.93, P = 0.041).Conclusions:Pre-illness CHIP was independently associated with increased mortality and morbidity in critically-ill adults with sepsis. These findings suggest that CHIP is a risk factor for sepsis severity. Elucidating the mechanism underlying this association could uncover new therapeutic interventions for sepsis.

Clonal hematopoiesis of indeterminate potential (CHIP) is associated with an elevated risk of hematologic and solid cancers. We performed a prospective cohort study, including 63690 patients with a first diagnosis of primary cancer in the UK Biobank during 2006 to 2022, to investigate the association of pre-diagnostic CHIP with future risk of second cancers. Cox regression was employed to assess the association between pre-diagnostic CHIP and risk of developing second cancer among patients with primary cancer. We identified 2860 patients with and 60626 without pre-diagnostic CHIP. During a median follow-up of 3.9 years, patients with primary cancer with pre-diagnostic CHIP experienced a greater risk of any second cancer (hazard ratio 1.3, 95% confidence intervals 1.2-1.5), compared with those without pre-diagnostic CHIP. Increased risk of any second cancer was mainly noted for patients with pre-diagnostic CHIP and primary myelodysplastic neoplasia, myeloproliferative neoplasms, non-Hodgkin lymphoma, or breast cancer. Regarding types of outcome (i.e., second cancer), the excess risk was particularly high for second myeloid malignancy and non-myeloid hematological malignancy. The risk for a second cancer was mainly observed in DNMT3A-, TET2-, SRSF2-, or JAK2-mutant CHIP. These findings suggest increased awareness of second cancer risk among patients with primary cancer and pre-diagnostic CHIP.

Clonal hematopoiesis of indeterminate potential (CHIP) is a common age-related condition that increases risk for cardiovascular disease. However, its relationship with stroke remains uncertain. To resolve these conflicting findings, we analyzed genomic and clinical data from 800 160 participants with genetic sequencing and medical records across 3 large-scale cohorts: the Vanderbilt BioVU biobank (United States; enrollment 2007-2022), the National Institutes of Health All of Us Research Program (United States; enrollment 2018-2023), and the UK Biobank (United Kingdom; enrollment 2006-2010). The median follow-up time was 4.4 years (interquartile range, 1.8-10.2) in BioVU, 1.9 years (interquartile range, 0.4-3.9) in All of Us, and 12.4 years (interquartile range, 11.7-13.1) in UK Biobank. Stroke events were identified and classified as ischemic or hemorrhagic using International Classification of Diseases codes. Subgroup analyses were conducted by driver gene, clone size, sex, and menopausal status. Genetically predicted levels of 27 cytokines were assessed for modification of CHIP-associated stroke risk. CHIP was associated with increased risk of incident stroke in the meta-analysis (hazard ratio [HR], 1.20 [95% CI, 1.14-1.27]; P=1.92×10-10). This association was observed for ischemic (HR, 1.18) and hemorrhagic (HR, 1.25) stroke subtypes. Gene-specific analyses showed strong associations for JAK2 (HR, 2.52) and TET2 (HR, 1.23). DNMT3A demonstrated weak but significant associations (HR, 1.13). CHIP was associated with stroke risk in both sexes; however, among women, the association was evident in postmenopausal (HR, 1.49 [95% CI, 1.16-1.92]; P=1.91×10-3) but not in premenopausal participants (HR, 0.70 [95% CI, 0.36-1.43]; P=0.33). Among participants with CHIP, but not among participants without CHIP, genetically predicted levels of IL-1RAP (interleukin-1 receptor accessory protein) were predictive of risk for stroke, suggesting IL-1RAP as a modifier of the CHIP-associated risk for stroke. Our large-scale, multicohort study establishes CHIP as a determinant of incident stroke risk and IL (interleukin)-1-mediated inflammation as a targetable pathway to reduce this risk.

GCA is the most common vasculitis after 50 years of age, responsive to steroids with frequent relapses. Our objective was to evaluate clonal haematopoiesis of indeterminate potential (CHIP) as a risk factor for relapse in GCA. We prospectively analysed CHIP in a monocentric cohort of recently diagnosed GCA patients. CHIP was defined as a variant in a gene implicated in myeloid malignancies with allele frequency >2% detected in peripheral blood mononuclear cells by next-generation sequencing. Relapses were defined as GCA related signs or symptoms and/or inflammatory syndrome attributable to GCA after remission induction. The primary outcome was relapse occurring within 12 months of GCA induction treatment. We included 40 patients with 20 women (50%) of median age 73 years [67-80]. At diagnosis, 16 (40%) patients had ophthalmic involvement and 23 (57%) patients had large vessel involvement. CHIP was detected in 18 (45%) patients. During a median follow-up of 26 [14-45] months, 17 (42%) patients relapsed at 12 months. In multivariate analysis, baseline factors independently associated with GCA relapse at month 12 were ophthalmologic involvement at diagnosis (OR 4.02, 95% CI [1.19-13.56], P < 0.025) and the presence of CHIP (OR 9.94, 95% CI [2.98-33.17], P = 0.0002). The presence of CHIP is associated with GCA relapses in this exploratory cohort. Further studies are needed to confirm these findings.