Upon activation with NF-κB, a spliced form called XPB-1 (S) is generated that successfully mediates estrogen-dependent and estrogen-independent resistance of BC; in addition, it also induces the up-regulation of various anti-apoptotic proteins including B cell lymphoma-2 (Bcl-2), HER2, Bcl-xl, Ras, c-Fos, c-Jun, and mutated p53 [69,72], and this suggests that NF-κB contributed to BC survival and resistance. This evidence concerns the gene TP53 and breast cancer.