H2AX and non-small cell lung carcinoma: Similar results were also observed in MGH119 cells, which were recently derived from a treatment-naïve, EGFR mutant NSCLC patient (21, 22), with respect to EGFR inhibitor-induced γ-H2AX formation, ATM activation, and ATM inhibitor-mediated sensitization to EGFR blockade (Fig. 3F and fig.