Whereas the reason for poor inhibition to FAK or IGF-IR activity in NSCLC is not clear, our findings indicated that TAE226 strongly inhibited the mutant EGFR, compared to FAK and IGF-IR, in cells that are “addicted” to the mutant EGFR, resulting in the anti-tumor activity of TAE226. This evidence concerns the gene IGF1R and non-small cell lung carcinoma.