Impairment of autophagy by TGF-β1 or IL-17A promoted fibrogenesis in pulmonary fibrosis [107, 108], while autophagy activation via IL-17A blockage decreased the production of collagen, attenuated fibrosis, and increased survival in the murine model of bleomycin-induced fibrosis [108]. The gene discussed is TGFB1; the disease is pulmonary fibrosis.