AKT1 and lung adenocarcinoma: Further analysis (Western blot) confirmed that FIP-nha induced a dose-dependent (0–16 μg/mL) decrease in the expression of both Akt (p-Akt) as well as mTOR (p-mTOR), thus confirming the critical role of PI3K/Akt pathway in A549 and H2347 lung adenocarcinoma cells.