As isoform switching between IDH1 and IDH2 mutations is a mechanism of acquired resistance to specific IDH inhibitors through the restoration of 2-HG levels [123], combined inhibition of both IDH isoforms or the use of dual IDH1/2 inhibitors, such as vorasidenib, could be a viable strategy to avoid the increase in 2-HG levels in AML cells. This evidence concerns the gene IDH2 and acute myeloid leukemia.