Future studies will determine whether the genetic inactivation of Snx27 or Vps35 leads to AQP4 depletion and if restoration of SNX27-retromer activity in vivo can be of therapeutic interest to stabilise AQP4 levels and rescue ventriculomegaly in Kidins220-deficient mice or in other hydrocephalus or neurological disease models that may concur with AQP4 deficiency. The gene discussed is VPS35; the disease is Hydrocephalus.