CPT2 and metabolic dysfunction-associated steatotic liver disease: MASLD is due to (a) hepatic fatty acid uptake derived from plasma free fatty acid (FFA) released from TG hydrolysis in adipose tissue [2], (b) hepatic de novo fatty acid synthesis regulated independently by insulin and glucose through the activation of SREBP-1c and ChREBP, respectively, and (c) transport of fatty acids into the mitochondria for oxidation, which is regulated by carnitine palmitoyl transferase (CPT1), carnitine translocase, and CPT2.