Silencing of BRCA1-induced phosphorylation of Ser536 site of p65 and p100/p52 activates the NF-κB canonical (p65/p50) and non-canonical pathway (p100/p52), nuclear translocation, p52/RelB coupling and proliferation of MCF1 breast cancer cell lines (Sau et al., 2016). This evidence concerns the gene NFKB1 and breast carcinoma.