The same study found that E2F1 and E2F2 could also act as upstream transcriptional repressors of CPT2 in nonalcoholic steatohepatitis-induced hepatocellular carcinoma and that low expression of CPT2 could provide the lipid-rich environment required for hepatocarcinogenesis [132]. The gene discussed is CPT2; the disease is metabolic dysfunction-associated steatohepatitis.