Aside from the well-known genetic alterations, such as EGFR and KRAS mutations or ALK and ROS1 rearrangements in lung adenocarcinoma, mutations or copy number variations of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway members also frequently occur in lung cancer and may also serve as therapeutic targets [9,10]. This evidence concerns the gene AKT1 and lung cancer.