In IPF lungs, it has been shown that TGF-β, VEGF, FGF, cytokines and chemokines (e.g., IL-13, CCL2), ROS, Wnt/β-catenin pathway, PI3K/AKT/mTOR pathway, Notch signaling pathway, ECM protein components, pulmonary arterial endothelial cell to mesenchymal transition (EnMT) and α-SMA are hypothesized as potential sources/mechanisms of myofibroblast activation, which contribute to lung fibrosis and lead to aberrant fibroblast proliferation and apoptosis of NSCLC cells [112]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.