Previous studies have proved that BMAL1 can strengthen p65 through recruiting CBP acetylation and activation of NF-κB [46], the CoIP assay found that BMAL1 can interact with CBP, overexpression of BMAL1 can increase the BMAL1-p65 compound CBP in abundance, as a result, BMAL1 can increase the recruitment of CBP to enhance p65 activity, and further enhance the expression of MMP9 target genes, promote the invasion and metastasis of breast cancer cells. Here, NFKB1 is linked to breast carcinoma.