In fact, it has been reported that in NSCLC, PI3K/AKT/mTOR signaling is most commonly disrupted due to multiple molecular impairments in this pathway, such as activation of mutations and/or overactivation of receptor tyrosine kinases (RTKs), activating mutations and/or amplifications of genes involved in PI3K, and inactivating mutations or deletion of the tumor suppressor PTEN [127,128,130,131]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.