In summary, though the activation of Src may have pleiotropic effects that depend on the cell type and context, our results clearly demonstrated that Rapamycin markedly enhanced the anticancer effect of Dasatinib by facilitating cell cycle arrest and repressing cell proliferation, invasion as well as migration through Src/PI3K/AKT/mTOR pathway, implying promising therapeutic benefit of mTOR/Src dual inhibition for NSCLC treatment. Here, AKT1 is linked to non-small cell lung carcinoma.