Animal and human experimental data have providedstrong evidence for establishing a pathophysiological link between PPAR and NAFLD.Although the molecular mechanisms remain unclearly defined, direct reciprocalinteractions between the virus itself and PPAR reinforce the hypothesis for the role ofthese transcription factors in the control of liver injury, particularly in steatosis,inflammation, and fibrosis. This evidence concerns the gene PPARA and metabolic dysfunction-associated steatotic liver disease.