As expected, inhibition of αVβ3 by the cyclo-RGD antagonist in combination with TMZ in the glioma xenograft model, led to pronounced tumor regression and showed consistently reinforced γH2AX phosphorylation and caspase-3 cleavage, strongly reduced Rad51 and RIP1 expression, and revealed a persistent IκBα expression in tumors in situ compared to mice treated with TMZ alone. Here, NFKBIA is linked to glioma.