More important, metformin can inhibit the expression of anti-apoptotic proteins such as Bcl-2 and Mcl-1 [23], In the present study, and as expected, metformin could effectively overcome the deficiency of vorinostat in regulating anti-apoptotic Bcl-2 family proteins, the addition of low-dose metformin could significantly inhibit Bcl-2, Bcl-xL and Mcl-1, and further enhanced the expression levels of BIM and BAX, and synergistically induced apoptosis and enhanced the sensitivity of gefitinib in these NSCLC cells. This evidence concerns the gene BCL2L11 and non-small cell lung carcinoma.