PPARGC1A and metabolic dysfunction-associated steatotic liver disease: While we have suggested that preserving mitochondrial function via SirT1/PGC1a signaling pathway is vital to the lipid-lowering effect of NAC, we still cannot exclude other possible involved mechanisms such as interfering entry of fatty acids or de novo lipogenesis in liver, and excessive fatty acid could trigger endoplasmic reticulum (ER) stress, which is a typical pathological process participating in the development of NAFLD.