This result complements the already reported findings by our group, where chemical V2r blockade by the selective antagonist tolvaptan completely abolished [V4Q5]dDAVP effects in MDA-MB-231 breast cancer cells (32) and, also, the findings by Keegan et al. (23), where the use of satavaptan (another non-peptidic V2r antagonist) blocked the mild cytostatic effects of dDAVP on human breast cancer cells. The gene discussed is AVPR2; the disease is breast carcinoma.