FASN and cancer: Given that acetyl-CoA is the substrate for mFAS and that (cytosolic) FASN can generate excessive amounts of free FAs that can be catabolized to acetyl-CoA [96, 97], it may be tempting to suggest that the FASN-driven abundance of FAs in cancer cells allows them to be an indispensable fuel source (in the sense that acetyl-CoA itself is catabolized) for mFAS-facilitated ETC assembly, cellular respiration, and downstream TCA function [98].