CPT1A and neoplasm: In this regard, PPARɣ induces FAO activation and overexpression of genes involved in lipid metabolism in cancer cells, such as pyruvate dehydrogenase kinase 4 (PDK4), carnitine palmitoyltransferase 1 (CPT1), and fatty acid binding proteins (FABPs) [102], supporting the tumor cells’ adaptation to a hypoxic and low nutrient tumor niche.