Currently, the known mechanisms of acquired resistance are as follows [13–17]: 1) the secondary gatekeeper EGFR T790M mutation which increases ATP affinity and subsequently prevents drug binding to the kinase domain; 2) activation of members of downstream signaling pathways such as RAS-RAF-ERK MAPK pathway and PI3K/AKT/mTOR pathway; 3) activation of bypass signaling through receptor tyrosine kinase such as MET; 4) changes in tumor histology with tumor cells displaying features of small-cell lung cancer or epithelial-mesenchymal transition (EMT). This evidence concerns the gene AKT1 and neoplasm.