In FLT3-mutated AML, this involves codifying type-I ↔ type-II tyrosine kinase inhibitor rotation upon detection of TKD/gatekeeper variants; in IDH-mutant disease, sequential or dual-isoform blockade at evidence of IDH1↔IDH2 switching (Lyu et al., 2020); and under venetoclax pressure, partner substitution (e.g., CDK9 or MAPK inhibitors) when BH3 profiling indicates a shift from BCL-2 to MCL-1/BCL-XL dependence (Kannan et al., 2025). This evidence concerns the gene FLT3 and acute myeloid leukemia.