Resistance-Driven Genotype-Therapy Matching: Small-molecule inhibitor combinations are optimized to target genotype-specific AML drug resistance nodes—e.g., FLT3-ITD (high allelic ratio) relies on quizartinib + MEK inhibitors to block gatekeeper mutations and RAS/MAPK bypass, while IDH-mutant AML uses ivosidenib + STING agonists to counter epigenetic reversion, directly addressing core resistance mechanisms. This evidence concerns the gene MAP2K7 and acute myeloid leukemia.