Given that the spoke head of RS3 is retained in the human PCD patients with RSPH1 mutation [17], the lack of all the triplet spoke heads in Rsph4a KO mice could explain the more severe structural defect of axoneme of respiratory cilia in RSPH4A patients than RSPH1 patients [16, 18]. This evidence concerns the gene RSPH1 and primary ciliary dyskinesia.