Whereas YC-1 treatment induced the downregulation of the NFκB/p65 activation by preventing IκBα degradation, and hence inhibiting the nuclear translocation of NFκB/p65 subunit [9]; iv) YC-1 blunts the increase in the downstream pro-angiogenic factors, which promote the exacerbation of subretinal NV; v) earlier studies have indicated that high concentrations of YC-1 inhibited NFκB/p65 activation and induced apoptosis in human prostate cancer cells [11]. Here, NFKB1 is linked to prostate cancer.