SLC12A2 and intracranial hemorrhage: Taken together, such lack of brain hemorrhage‐induced increase in [K+]CSF is at odds with the recently proposed K+‐induced NKCC1‐mediated reversal, promoting choroid plexus as a site of CSF reabsorption following brain hemorrhage.[40] Rather, the stable [K+]CSF obtained in the present patient cohort suggests that NKCC1 retains its net outward transport direction and its continued contribution to CSF secretion during a hemorrhagic event.