Underlying these abnormalities is a wide range of disorder of nuclear transcription factors that adjust lipid metabolism, inflammation, and fibrogenesis, which consist of CD36; peroxisome proliferator-activated receptor- (PPAR-) α, PPAR-δ, and PPAR-γ; farnesoid X receptor (FXR); and sterol regulatory element binding protein 1 (SREBP-1), which are ideal targets for NAFLD treatment [152, 153]. This evidence concerns the gene CD36 and metabolic dysfunction-associated steatotic liver disease.