Deletion of either E2 elicited stronger growth inhibitory effects in the AML cells that were more dependent on MARCH5, particularly in cultured cells from a CRISPR-competent patient-derived xenograft (PDX) model of AML (PDX17-14, complex karyotype with an MLL-AF10 fusion) [5] (Fig. 1d). The gene discussed is KMT2A; the disease is acute myeloid leukemia.