As reported previously [30] our observations have both basic as well as significant clinical relevance: (a) it identifies a molecular regulator, which may be critical in breast cancer cell–specific CNKSR2 overexpression (b) it also identifies Smurf2 as a novel therapeutic target, down-regulation of which can degrade CNKSR2 protein leading to reduced proliferation of breast cancer cells. This evidence concerns the gene SMURF2 and breast carcinoma.