Further study showed that low membrane-associated PTEN distribution probably resulted from the decreased expression of caveolin-1 that interacted with caveolin-1-binding sequence in PTEN and thus regulated the membrane levels of PTEN [98] suggesting that caveolin-1 is the key therapeutic target to inhibit IPF by regulating PTEN activity. The gene discussed is PTEN; the disease is idiopathic pulmonary fibrosis.