Treating NSCLC with EGFR-TKI would enrich c-Met-positive tumor cells, with the overexpression and overactivation of c-Met consequently triggering the activation of Her3, thus activating downstream signal transduction molecules such as Akt and Erk, independent of EGFR kinase activity [4, 5], and finally switching to the c-Met pathway to control tumor growth [21]. This evidence concerns the gene AKT1 and neoplasm.