IL-17-deficient (IL-17-/-) mice can be protected from NASH evolution, as indicated by decreased c-Jun N-terminal kinase (JNK) activation, reduced phosphatase and tensin homolog (PTEN) expression (Phosphatidylinositol 3-kinases (PI3K) inhibitor), and improved Akt phosphorylation compared to wild-type mice, accompanied by extensive liver Th22 lymphocyte infiltration. The gene discussed is PTEN; the disease is metabolic dysfunction-associated steatohepatitis.