As shown in Figure 9A, expression of γH2AX and cleaved caspase-3, as well as reduction in Rad51 and RIP1 expression and sustained level of IκBα expression were significantly more enhanced in tumor extracts from animals treated with the inhibitor and TMZ, in comparison to non-treated mice and mice treated with the RGD inhibitor or TMZ only, revealing the same molecular mechanism to occur also in vivo. The gene discussed is NFKBIA; the disease is neoplasm.