Abstract
An improved understanding of the biology underlying leukemogenesis, including the determination of the cells of leukemia origin, is of great importance as it can have immediate implications on patient treatment and management. The article by Riemke et al ([2016][1]) provides further evidence that a subgroup of acute myeloid leukemia (AML), the most common acute leukemia in adults, might arise from T‐lymphoid progenitor cells. This study not only supports that the lymphoid fate of early T‐cell progenitors is not yet fully stabilized but also shows that under oncogenic conditions, this multilineage plasticity potential of T‐lymphoid progenitors can lead to transdifferentiation into myeloid leukemia. While gene expression profiles suggest that approximately 5% of all AML cases originate from T‐lymphoid progenitors, novel treatment strategies targeting JAK2/STAT3 signaling might open new avenues for this AML cohort. [1]: #ref-7
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