This finding, alongside the uniformly downregulated expression of PCDH9, ISLR2, ADAMTSL2, and B4GAT1 in our iNPH patients, reinforces the potential parallel mechanisms in the pathophysiology of congenital hydrocephalus and iNPH and raises the possibility that iNPH may be a forme-fruste of congenital hydrocephalus that manifests in adulthood at least in a subset of patients. This evidence concerns the gene PCDH9 and congenital hydrocephalus.