These studies showed that IPF fibroblasts have acquired a desensitizing mechanism to respond to environmental stress such as polymerized collagen matrix by utilizing the PTEN/Akt/mTOR axis, and this pathologically altered autophagic pathway may be responsible for the IPF fibroblast's ability to maintain a viable phenotype on collagen rich matrix. This evidence concerns the gene AKT1 and idiopathic pulmonary fibrosis.