First, similar to ATM-deficient cells from ataxia telangiectasia (A-T) patients (34, 35), silencing of EphA5 in lung cancer cells in vitro caused severe defects in IR-induced G1-S cell cycle checkpoint and increased sensitivity to IR, suggesting that EphA5 may be participating in DDR as a component with ATM, well known to be a central kinase in DDR function(s) (36). This evidence concerns the gene EPHA5 and lung cancer.