In addition, overexpression of follistatin, (FST), a gonadal protein that specifically inhibits follicle-stimulating hormone release, alleviated lipid accumulation and lipogenesis, whereas FST knockdown aggravated hepatic steatosis via suppressing the mTOR pathway, therefore, may have a potential to become a therapeutic target in NAFLD/NASH [137]. This evidence concerns the gene MTOR and metabolic dysfunction-associated steatohepatitis.