KMT2A and acute myeloid leukemia: Its mechanism of action is mainly to disrupt the binding of Menin to the binding pocket in MLL1/2 and MLL1-FP, thereby reducing the binding of MLL1/2 and MLL1-FP to their targets, inhibiting HOXA9/MEIS1 activity, and inducing differentiation and loss of viability of AML with MLL1-r or mutant (mt)-NPM1 [81].