We previously reported the identification of recurrent heterozygous CWH43 deletions in 15% of patients with shunt-responsive iNPH and showed that genetically engineered mice that were heterozygous or homozygous for one of these iNPH-associated CWH43 deletions develop an iNPH-like syndrome characterized by communicating hydrocephalus and impairments in gait and balance (20). Here, CWH43 is linked to communicating hydrocephalus.