The results showed that β1 integrin interacted with polymerized collagen and suppressed normal fibroblast proliferation through PI3K/Akt/S6K1 pathway owing to the enhanced lipid phosphatase activity of PTEN, whereas IPF-derived fibroblasts had low lipid phosphatase activity that resulted in high activity of PI3K/Akt pathway [99]. Here, AKT1 is linked to idiopathic pulmonary fibrosis.