Specially in NSCLC, EMT plays pivotal roles in the acquired resistance to EGFR-TKIs such as gefitinib.3, 4 For example, restoring E-cadherin expression or silencing EMT regulator Slug increases gefitinib sensitivity in NSCLC cells with a mesenchymal phenotype.5, 6 Accumulating evidences indicate that constitutively activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling is a central feature of EMT in many cancers including NSCLC.7, 8 However, the exact mechanism for the acquired gefitinib resistance of NSCLC remains unclear. This evidence concerns the gene AKT1 and cancer.