Nevertheless, our main goal of this study was to examine whether enhanced Akt/mTOR suppresses LC3-2 expression in most IPF fibroblasts on collagen and we found that when IPF fibroblasts interact with collagen rich matrix, the alteration of a Akt/mTOR axis can contribute to the desensitization of IPF fibroblasts to the stress inducing effects of polymerized collagen. Here, AKT1 is linked to idiopathic pulmonary fibrosis.