Interestingly, although deletion of P53, a key executor of DDR, partially rescues the Ataxia phenotype in Nbs1-CNSΔ (Frappart et al., 2005), γ-H2AX foci formation was abolished in Purkinje cells and surrounding granule cells in the absence of NBS1 (Figure 2A). This evidence concerns the gene H2AX and Ataxia.