We have reported (Medova et al., 2010) that in MET‐overexpressing human gastric adenocarcinoma cells GTL‐16, inhibiting MET with the small molecule PHA665752 16 h prior to IR treatment led to a substantial increase in the phosphorylation levels of both H2AX S139, a prominent substrate of ATM, ATR, and PRKDC (Friesner et al., 2005; Stiff et al., 2004), and ATM S1981, a marker of the activated form of this kinase (Shiloh and Ziv, 2013). The gene discussed is MET; the disease is gastric adenocarcinoma.