IDH2 and acute myeloid leukemia: Although the relatively high proportion of patients with cytogenetically normal AML limits the prognostic and clinical utility of these cytogenetically defined groups[11], recent advances in the understanding of the molecular landscape of AML have simultaneously expanded our prognostic ability and facilitated the development of agents targeting specific actionable alterations, including mutations of fms-like tyrosine kinase 3 (FLT3) and isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2)[15-17].