In in vitro and in vivo preclinical models of NSCLC harbouring KRAS mutations, ionizing radiation leads to FAK activation (Tyr397 phosphorylation), which persists for several hours, while the inhibition of FAK activity leads to an inherent loss of DNA repair capacity and radiosensitizing effects that promote the therapeutic effect of ionizing radiation [213,214,216]. This evidence concerns the gene PTK2 and non-small cell lung carcinoma.