A 23-year-old woman was referred at 32 weeks' gestation because of the fetal ultrasound finding of a large forehead mass. The pregnancy was initially uncomplicated and fetal ultrasound examinations at 12, 16 and 19 weeks' gestation were all normal. Sonography at 32 weeks (Figure 1a) showed a mass over the mid-forehead just above the nasal bridge, with slightly amorphous content, measuring 4.1 × 4.0 × 3.1 cm. It did not appear to penetrate the scalp or the skull, and no brain abnormalities were seen. There were some blood vessels supplying the tumor, emerging from the scalp. Fetal magnetic resonance imaging confirmed the findings (Figure 1b). The couple received counseling and decided to continue the pregnancy. Sagittal ultrasound (a) and magnetic resonance (b) images demonstrate the midline pedunculated forehead mass and confirm the lack of intracranial extension. No subjacent intracranial abnormalities were detected. Doppler examination (not shown) demonstrated scalp vascularity. (c, d) Postnatal photographs showing the infant's forehead tumor. Delivery was at 38.8 weeks by Cesarean section. The neonate's growth parameters were all normal. The Apgar scores were 9 and 10 at 1 and 5 mins, respectively. Examination showed a pedunculated tumor measuring 5 × 3.5 × 2.5 cm with a large base (Figure 1c and d), originating in the mid-right side of the forehead with areas of skin necrosis and excoriation. No other abnormalities were detected on examination. Complete resection was performed 7 days after birth, and follow-up at 18 months of age showed normal growth and development and no recurrence of the tumor. Histopathology showed a spindle cell tumor with a diffuse hemangiopericytomatous growth pattern and a variable collagenous background. There was no architectural zonation. Cords of plump spindle cells were separated by thin vascular channels, and ‘staghorn-shaped’ dilated vascular spaces were present in areas (Figure 2a and b). The tumor cells demonstrated diffuse positive cytoplasmic immunohistochemical staining for vimentin and focal positive staining for S100 and smooth muscle actin. There was diffuse pericellular immunohistochemical staining for collagen IV (Figure 2c). Vascular markers CD31 and CD34 highlighted an extensive fine capillary network between the cords of cells (Figure 2d). Interphase fluorescent in situ hybridization (FISH) analysis with a dual color break-apart probe for the ETV6(TEL) gene (12p13) showed absence of an ETV6 re-arrangement, and reverse transcription–polymerase chain reaction (RT-PCR) did not detect the t(12;15)(p13;q25) reciprocal translocation associated with congenital fibrosarcoma (Figure 2). Tumor histology. (a) Dilated ‘staghorn’ vascular spaces within the cellular tumor (hematoxylin and eosin (H&E) stain, original magnification × 50). (b) Mitotically active, but cytologically bland, tumor cells (H&E stain, original magnification × 200). (c) Pericellular immunohistochemical staining for collagen IV (Dako Denmark A/S, Glostrup, Denmark; original magnification × 200). (d) Perivascular distribution of tumor cells highlighted by immunohistochemical staining of vascular endothelial cells with CD31 (Dako Denmark A/S; original magnification × 200). Hemangiopericytoma (HPC) is a rare form of vascular tumor that was first recognized in 19421. Infantile HPCs are usually benign and are distinct from adult HPCs, which are aggressive and even malignant. About 5–10% of cases of HPC occur in children, and around one-third of these present during the first year of life2, 3. Common locations include the head and neck region, lower extremities and retroperitoneum. Microscopically, many soft tissue tumors in children demonstrate hemangiopericytomatous patterns, and infantile HPC has been challenged as being a specific entity4, 5. As the benign behavior is similar to that of other soft tissue tumors in infancy (e.g. congenital infantile fibrosarcoma and infantile myofibromatosis), a single entity called composite myofibromatosis has been proposed to encompass all these different tumors6. However, its typical clinicopathological features continue to clinically warrant recognition of infantile HPC as a distinct entity7. Other important differential diagnoses of infantile HPCs include neurofibroma, leiomyomas, hyaline fibromatosis, hemangiomas, soft tissue sarcoma and metastatic neuroblastoma8. Complete surgical resection is the treatment of choice. Aggressive resection and radiotherapy are often not required because of its sensitivity to chemotherapy2, 3. Long-term follow-up is recommended as relapse may occur later. H. Y. B. Chung* ¶, L. Chu , C. Forrest§, R. Silver¶, A. Toi**, S. Blaser , S. Viero , G. Taylor , D. Chitayat* ¶, * The Hospital for Sick Children, Department of Pediatrics, Division of Clinical and Metabolic Genetics, UK, The Hospital for Sick Children, Department of Pediatrics, Division of Neuroradiology, UK, The Hospital for Sick Children, Department of Pediatrics, Division of Pathology and Laboratory Medicine, UK, § The Hospital for Sick Children, Department of Pediatrics, Division of Plastic Surgery—The Craniofacial Program, Mount Sinai Hospital, UK, ¶ Department of Obstetrics and Gynecology, The Prenatal Diagnosis and Medical Genetics Program, Toronto, Ontario, Canada, ** University Health Network, Department of Medical Imaging, University of Toronto, Toronto, Ontario, Canada