On the other hand, Fas/CD95 has been recently reported to interact with Kip1 ubiquitination-promoting complex protein 2 (KPC2) in triple-negative breast cancer cells, independently of FasL/CD95L, and leads to the partial degradation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), thus suppressing NF-κB-driven gene expression [23], and pointing out the interplay of Fas/CD95 death receptor with an important cell survival signaling. This evidence concerns the gene NFKB1 and triple-negative breast carcinoma.