Id-1 promotes survival of prostate cancer cells through the NF-κB pathway (Ling et al, 2003), and it regulates the apoptotic response of cancer cells towards various chemodrugs (Zhang et al, 2007b), such that inactivation of Id-1 results in increased sensitivity of prostate cancer cells to paclitaxel through the JNK pathway (Zhang et al, 2006). This evidence concerns the gene NFKB1 and prostate carcinoma.