Mechanically, SIRT1 can participate in the occurrence and development of NAFLD by affecting signal molecules such as PGC-1α and SREBP-1c, FoxO1/3, STAT3, and AMPK, and restore the function of mitochondria by regulating mitochondrial fat oxidation and reducing the production of ROS, thus controlling the progress of NAFLD. This evidence concerns the gene PPARGC1A and metabolic dysfunction-associated steatotic liver disease.