KCa3.1 channels have been reported to be up-regulated in disease states characterized by abnormal cell proliferations such as neointima formation [6,7] and organ fibrosis [8], and, important for the present study, in several solid cancers; prostate, hepatocellular carcinoma, endometrial, mammary carcinoma and glioblastoma [9–14], several cancer cell lines [15–19], tumor vessels, proliferating endothelial cells [20,21], and activated T cells [22–25]. This evidence concerns the gene KCNN4 and breast carcinoma.