FBXW7α specifically recognizes residues T2512/P2513 in the cdc4-phosphodegron of the nuclear molecules NICD1 and NICD4, while highly expressed prolyl-isomerase1 (Pin1) competitively binds to the site where NICD1/NICD4 docks with FBXW7α, disrupting the feed-forward molecular circuit between the three, inducing breast carcinogenesis and promoting breast cancer stem cell (BCSC) self-renewal [17]. This evidence concerns the gene FBXW7 and breast cancer.