The mammalian brain is bathed in the cerebrospinal fluid (CSF), which is continuously secreted by the choroid plexus located in each of the four ventricles. The CSF production has generally been assumed to take place by transepithelial transport of ions followed by osmotically obliged, passive movement of water, partly via the water channel aquaporin 1 (AQP1) expressed at the luminal membrane of the choroid plexus. The limitations of such a conventional osmotic model for CSF production are apparent from 1) the lack of osmotic driving force across the choroid plexus epithelium, 2) the minimal effect of genetic deletion of AQP1, and 3) the ability of the choroid plexus epithelium to transport water uphill against a transepithelial osmotic gradient. A number of cotransporter proteins have the inherent ability to cotransport water along with the ions/solutes in the translocation mechanism in a manner that permits water to be transported independently of an osmotic gradient. This talk will introduce the water-translocating Na⁺,K⁺,2Cl^- cotransporter, NKCC1, as a key contributor to CSF production in the murine choroid plexus. The NKCC1 cotransport protein is located in the luminal membrane of the choroid plexus and is poised for ion and water transport from the choroid plexus epithelial cell to the ventricle. With its inherent ability to transport water along with the ion translocation, NKCC1 is able to move water independently of the osmotic gradient and in this manner contribute approximately half of the CSF secretion across the luminal membrane.