These inhibitors are unlikely to provide cure of the AML due to primary resistance from co-mutations in other pathways especially the NRAS/KRAS, and MAPK pathway effectors PTPN11, NF1, FLT3 and others [38] and secondary resistance from development of second-site IDH2 missense mutations or isoform switching [39, 40]. Here, IDH2 is linked to acute myeloid leukemia.