PKM and cancer: However, the issue of the supply of AcCoA for fatty acid synthesis in glycolytic cancer cells is still unresolved, since AcCoA production from pyruvate in cancer cells is often reduced due to: i) a switch from pyruvate kinase (PK) M1 to the less active PKM2 that reduces pyruvate production [25, 26] and ii) a decreased entry of pyruvate into the TCA cycle due to inactivation of pyruvate dehydrogenase (PDH) [27], which can be compensated by the entry of pyruvate into the TCA cycle via the anaplerotic conversion to oxaloacetate by pyruvate carboxylase (PC) [28] or glutamine catabolism [29–31].