Preclinical studies indicated that Met inhibits PI3K/AKT/mTOR signaling and IGF-1R [23–25], and combination of Met with gefitinib markedly reduces the proliferation of NSCLC cell-lines harboring the wild-type LKB1 gene by inducing LKB1-mediated activation of AMPK, which in turn inhibits mTOR signaling [26]. Here, IGF1R is linked to non-small cell lung carcinoma.