AKT1 and pulmonary fibrosis: Immunohistochemical (IHC) analysis of fibroblasts within the fibroblastic foci of IPF patient specimens also revealed that PTEN, caveolin-1 (cav-1) and forkhead box O3a (FoxO3a) expression are all suppressed, while AKT activity is upregulated, further supporting the importance of the PTEN-PI3K/AKT axis in the pathogenesis of pulmonary fibrosis [26,27].