We speculate that further contributing and overlapping mechanisms are probable, including the ability of cooperative IL8 and VEGF signaling to stimulate key transcriptional programs including that of the AR, NF-κB, and HIF-1, resulting in a broad and sustained intrinsic modulation of pro-tumorigenic, resistance-associated, and proliferation-driving genes in tumor and vascular endothelial cells resident within the hypoxic zone (11). Here, NFKB1 is linked to neoplasm.