In mice treated with DEN and exposed to a high-fat, high-cholesterol and high-sugar diet (HF-HC-HSD), which triggers liver fibrosis, it has been observed that the increase in HIF-1α coupled with the release in inflammatory cytokines mediated metabolic reprogramming, angiogenesis and proliferation, thereby prompting switching from NASH to HCC [118,119]. The gene discussed is HIF1A; the disease is metabolic dysfunction-associated steatohepatitis.