Similarly, mutations in human ODAD1 typically result in the absence of ODA and almost complete ciliary immotility, and result in a typical PCD clinical phenotype, including a high incidence of neonatal respiratory distress, low levels of nasal nitric oxide, sinusitis, otitis media, bronchiectasis, and situs inversus totalis [17,18]. This evidence concerns the gene ODAD1 and Neonatal respiratory distress.