For example, AML resistance can be acquired through the upregulation of BCL2A1 and CLEC7A, mutations in PTPN11 and KRAS [52], upregulation of the mitochondrial chaperonin CLPB [53], and inactivation of TP53, BAX, and PMAIP1 genes [54]. This evidence concerns the gene KRAS and acute myeloid leukemia.