Antitumor effects of KCa3.1 inhibition were correlated to suppression of cell proliferation and migration in breast cancer, endometrial carcinoma and hepatocellular carcinoma cells.33, 34, 35 In combinations, it increased the sensitivity of glioblastoma cells for radiotherapy36 and of glioma cells for temozolomide.37 In most instances, KCa3.1 blockers were cytostatic rather than cytotoxic or proapoptotic,33, 38 which may limit their use as monotherapy but may encourage for combination with proapoptotic agents. The gene discussed is KCNN4; the disease is endometrial carcinoma.