The hepatoprotective properties of IL-22 are also observed in NAFLD and are majorly mediated by stimulating STAT3 phosphorylation, increasing PTEN and preventing PI3K/Akt activation, followed by modulating downstream gene expression, including antiapoptotic, antioxidative and lipogenic genes in hepatocytes, while evidence indicates that it is effective only in the absence of IL-17 [28,34,58]. This evidence concerns the gene IL17A and metabolic dysfunction-associated steatotic liver disease.