Additionally, UBE2J2 or UBE2K deletion increased venetoclax sensitivity even in the NOXA-null cells of multiple AML models, including another PDX-derived model cultured briefly in vitro (PDX16-01, with CALM-AF10 fusion, NF1, PHF6 and TP53 mutations) (Fig. 2i, j and Supplementary Fig, 2a–d). This evidence concerns the gene UBE2J2 and acute myeloid leukemia.