Since Src and IGF-1R are coactivated in most NSCLC cell lines and tumors in patients [18] and plays an important role in cancer cell survival and resistance to targeted anticancer therapies [50, 51], and cancer cells appear to display resistance to the IGF-1R-targeted agents through Src activation [17, 18], we postulated that dual targeting of IGF-1R and Src could be an effective way to overcome anticancer drug resistance and dual IGF-1R/Src TKI regimens may offer a novel opportunity for cancer therapy. This evidence concerns the gene SRC and non-small cell lung carcinoma.