With regard to the importance of PI3K and p38 MAPK in the pathogenesis of fibrosis, it was shown that phosphorylated AKT is strongly expressed in areas of pulmonary fibrosis after intratracheal administration of bleomycin in mice, and that blockade of PI3K-AKT signaling attenuates pulmonary fibrosis induced by bleomycin treatment or TGF-β overexpression [43,44]. This evidence concerns the gene AKT1 and pulmonary fibrosis.