Although the exact mechanism of PPARs in lung fibrosis and lung cancer is largely unknown, a PPARγ agonist has been found to exert antitumorigenic effects in both IPF and lung cancer by inhibiting myofibroblast differentiation and activating phosphatase and tensin homolog (PTEN) [42, 43], consistent with our study, highlighting the importance of the PPAR pathway in lung cancer associated with IPF. Here, PTEN is linked to lung carcinoma.