Based on the data obtained in green algae, it seems that the extent of the defects in the cilia ultrastructure that translates into cilia immotility and the severity of the PCD symptoms in patients with mutated CCDC39 or CCDC40 genes is a consequence of the dysfunction of the mutated proteins as a determinant of the docking/positioning of three important ciliary complexes. This evidence concerns the gene CCDC40 and primary ciliary dyskinesia.