Interestingly, the current study not only observed that the upregulated RHBDL2 transcription was associated with worse DFS of breast cancer patients in TCGA, but also found that RHBDL2 silencing inhibited the YAP1/NF-κB signaling by upregulating USP31 expression and attenuated the spontaneous conversion of CD44-/CD24- cells into CD44+/CD24- CSCs and their mammosphere formation. This evidence concerns the gene NFKB1 and breast carcinoma.