The heterozygous loss of KMT2C could promote AML formation in mice.[8] KMT2C and KMT2D are large scaffold proteins that form the KMT2C/D COMPASS complex (complex of proteins associated with Set1), which contains WDR5, RBBP5, hDPY30, ASH2, KDM6A (UTX), PTIP, PA1, and NCOA6.[9] Besides KMT2C, it is also reported that loss‐of‐function mutations of KDM6A, which happened in AML, promoted myeloid leukemogenesis and contributed to chemotherapy resistance.[10, 11]. The gene discussed is DPY30; the disease is acute myeloid leukemia.