On the contrary, mtIDH1/2 inhibitor-induced differentiation may further increase venetoclax activity on IDH1/2mt cells by lowering the apoptotic threshold, as has been observed with other agents that promote differentiation.87 In vitro and in vivo experiments with an erythroleukemia cell line and primary AML samples suggested that enasidenib-induced differentiation further sensitizes IDH2mt AML cells to venetoclax, but that venetoclax might be antagonized by enasidenib when it fails to induce differentiation when administered as enasidenib monotherapy. Here, IDH1 is linked to acute myeloid leukemia.