MAX and neoplasm: Our data show that cMYC-MAX is an opportune therapeutic target for manipulating the TAM population away from tumor-promoting macrophages and that a small molecule antagonist, modified into a phosphatidylcholine prodrug, protected the compound from metabolism during circulation and allowed a unique αvβ3 NP delivery mechanism (CFDD) to circumvent enzymatic degradation within the phagocytosis pathway and discharge directly into the intracellular membranes.