LSD1 and DOT1L therapies exemplify a broader AML treatment principle: rewriting the chromatin state to unlock lineage maturation, then pairing with BH3 mimetics (e.g., venetoclax) or kinase inhibitors (e.g., FLT3 inhibitors) to convert differentiation into durable disease clearance. This evidence concerns the gene KDM1A and acute myeloid leukemia.