Repression of TP73 in IDH1/IDH2-mutant AML and downregulation of TP73 by the oncometabolite 2-HG were associated with enhanced sensitivity to venetoclax, thus supporting the view that TP73 determines AML susceptibility to BCL-2 inhibition; in contrast, venetoclax resistant AML cells overexpress TP73 and TP73 knockdown in these cells restores venetoclax resistance [144]. This evidence concerns the gene IDH1 and acute myeloid leukemia.