Since we recently identified the latter protein, Daple, as a proximity partner of wild-type more than a salt-bridge disrupting mutant α-cat77, and loss of other zAJ proteins or αcat proximity-partners can lead to hydrocephalus in mice89–91, we speculate that Ctnna14A/4A mice develop hydrocephalus through perturbing a particular feature of neuroepithelial zAJ integrity, which forms a critical barrier between brain cortex and fluid-filled ventricles. This evidence concerns the gene CCDC88C and Hydrocephalus.