Metabolic plasticity of AML LSC nevertheless allows for an escape from metabolic pressure of venetoclax treatment by an increase in fatty acid oxidation (FAO) that continues to drive enhanced OxPhos when amino acid metabolism is inhibited leading to resistance to venetoclax/azacitidine treatment protocol (44, 45), confirming previous experimental results that simultaneous pharmacological inhibition of FAO enhances sensitivity of AML cells to Bcl-2 inihibiton (46). Here, BCL2 is linked to acute myeloid leukemia.