Since Akt is an important kinase involved in negative regulation of autophagy via mTOR [26]–[28], [30], these data further suggest that the aberrant PTEN/Akt axis in IPF fibroblasts suppresses autophagy induction, thereby maintaining the pathological IPF fibroblast phenotype on polymerized collagen. The gene discussed is AKT1; the disease is idiopathic pulmonary fibrosis.