As mentioned in the previous section, AML with KMT2A rearrangement (KMT2Ar) is pathologically characterized by upregulated HOXA9 and MEIS1 genes, which are dependent on the interaction of oncogenic KMT2A fusion proteins with other complex-forming proteins such as LEDGF, DOT1L, and menin. Here, HOXA9 is linked to acute myeloid leukemia.