PI3K/Akt pathway is known to play a prominent role in driving EMT and drug resistance in cancers.23 It has been reported that activation of PI3K/Akt signaling could directly increase Cx43 phosphorylation24 and Cx43 also could contribute to activation of PI3K/Akt signaling.25 Therefore, we sought to determine whether there exists a reciprocal activation between Cx26 and PI3K/Akt pathway in promoting EMT and acquired gefitinib resistance of NSCLC cells. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.