We previously reported that, in patients with nonalcoholic steatohepatitis (NASH), CPT2 downregulation-mediated suppression of FAO not only enables hepatocellular carcinoma (HCC) cells to escape lipotoxicity, but also promotes hepatocarcinogenesis through the accumulation of acylcarnitine as an oncometabolite [49]. Here, CPT2 is linked to metabolic dysfunction-associated steatohepatitis.