The ataxia–telangiectasia (A–T) patient-derived lymphoblastoid cell line (LCL) (HA56) showed more γ-H2AX and 53BP1 foci at +1 h (p = 0.0131 and p = 0.1049) than the wildtype control line (HA325) and a significantly higher number of residual γ-H2AX and 53BP1 foci at +24 h (p < 0.0001 and p = 0.0112, respectively) (Figure 1). The gene discussed is H2AX; the disease is ataxia telangiectasia.