Given the evidence that activation of the E2F1-E2F2-CPT2 axis in nonalcoholic fatty liver disease (NAFLD)-related HCC promotes a lipid-rich environment conducive to HCC progression, alongside the observed stimulation of increased lipogenesis in various cell lines under hypoxic conditions within the HCC microenvironment [32, 33], we hypothesize that the HCC microenvironment as a whole remains highly enriched in lipids, notwithstanding the state of heightened lipid uptake, synthesis, and metabolism in HCC cells. This evidence concerns the gene CPT2 and metabolic dysfunction-associated steatotic liver disease.