Moreover, these NAFLD-like mechanisms of steatogenesis apply to all HCV genotypes with a few proposed differences where G-3 CHC seemingly amplifies steatogenic molecular mechanisms associated with NAFLD through significant changes in MTP, PPAR-α, SREBP-1c, and phosphate and tensin homolog (PTEN) [92]. The gene discussed is PTEN; the disease is metabolic dysfunction-associated steatotic liver disease.