The suppression of IGF-1R with a TKI leads to the utilization of alternative pathways of Src activation, most likely via various membrane-associated receptors, resulting in resistance to the drug (Fig. 6b); 3) suppression of IGF-1R with a TKI induces the posttranslational reprogramming of cells to activate cellular machinery to stabilize the Src and IGF-1R proteins in NSCLC cells with low levels of IGF-1R and Src co-activation, leading to the enhanced reciprocal co-activation of Src and IGF-1R and resistance to the drug (Fig. 6c). This evidence concerns the gene IGF1R and non-small cell lung carcinoma.