Experiments performed in primary human AML cells demonstrated that mutations in IDH1 or IDH2 genes induce dependence of AML cells on the antiapoptotic protein BCL-2 and, thus, higher sensitivity to venetoclax [87], a specific BCL-2 inhibitor that is already approved by the FDA for the treatment of AML in combination with hypomethylating agents, such as azacitidine [88,89]. Here, IDH2 is linked to acute myeloid leukemia.