Specifically, in non-small cell lung cancer cells, overexpression of FAPα significantly enhanced cell adhesion and migratory capacity, which was effectively attenuated by pharmacological inhibition of the PI3K pathway, as further confirmed by increased Akt phosphorylation observed in western blot analysis, indicating activation of PI3K/Akt signaling [86]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.