Nonetheless, mechanistically, the summarized evidence supports the notion that NAC could block lipid accumulation by the downregulation of SREBP-1c/SREBP-2 [44] or that of cluster of differentiation 36 (CD36) [45] and PPARγ, while enhancing intracellular antioxidant levels [46] in experimental models of NAFLD. The gene discussed is PPARG; the disease is metabolic dysfunction-associated steatotic liver disease.