In contrast, PPARα exhibited a low level of expression, and transcriptional promotion of CPT2 in hepatocellular carcinoma driven by obesity and nonalcoholic steatohepatitis could partially explain the downregulation of CPT2 expression, which was shown to be able to lead to hepatocellular carcinoma cell resistance to lipotoxicity through inhibition of Src-mediated JNK activation and to play a pro-cancer role through acylcarnitine accumulation exerting pro-cancer effects [131]. Here, CPT2 is linked to metabolic dysfunction-associated steatohepatitis.