Phosphorylation at ser-139 residue on histone 2A (γh2AX), a marker of DSB formation, was increased in patient derived cell lines from newly diagnosed GBMs cells upon TMZ treatment, while patient derived cell lines from recurrent GBM did not alter h2AX phosphorylation in the presence of TMZ (Figure 3A). This evidence concerns the gene H2AX and glioblastoma.