Therefore, the findings from the current study indicated that RHBDL2 promoted the spontaneous conversion of CD44-/CD24- cells into CD44+/CD24- CSCs by enhancing YAP1 stability through inhibiting its phosphorylation to suppress USP31 expression, enhancing the NF-κB signaling in breast cancer cells, whereas RHBDL2 silencing had the opposite effects in breast cancer cells (Figure 7G). This evidence concerns the gene NFKB1 and breast cancer.