The molecular coupling between the hemorrhagic event and the hydrocephalus formation was proposed to rely on the associated inflammatory response activating the Toll-like Receptor 4 (TLR4) signalling pathway, which ultimately promoted hyperactivity of the choroidal Na+/K+/2Cl− cotransporter NKCC1 [6], that serves as a key contributor to CSF formation by rodent and canine choroid plexus [6, 20–22]. Here, SLC12A2 is linked to Hydrocephalus.