HYDIN and Hydrocephalus: It has been demonstrated that cilia-related gene deletion of Foxj1 (Hfh4), Mdnah5 (dynein heavy chain), Polaris (Ift188), Hydin, Spag6 (central pair-dynein adaptor), and Tg737 (component of the intraflagellar transport particles) in mice all exhibited ependymal cilia structural and/or functional defects associated with hydrocephalus [39–43].