Two independent groups recently reported that Setd2 is indispensable for the self-renewal of HSCs and differentiation of myeloid as well as erythroid lineages36,37: deletion of exon 1 of Setd2 at results in defective hematopoietic-repopulating activity of HSCs and a myelodysplastic syndrome-like phenotype37; ablation of exon 6 of Setd2 dramatically decreases the population of HSCs and leads to leukopenia, anemia, erythroid dysplasia, and increased thrombopoiesis36. Here, SETD2 is linked to anemia.