One of the possible reasons why the IFT-B complex has not been as commonly associated with human ciliopathy phenotypes as the IFT-A complex, is its crucial role in ciliogenesis, as evidenced by embryonic lethality in many established mutant mouse models.7, 8 The IFT-B complex consists of a nine-subunit salt-stable core (IFT88, IFT81, IFT74, IFT70, IFT52, IFT46, IFT27, IFT25, IFT22/RABL5) and five peripheral components (IFT172, IFT80, IFT57, IFT54/TRAF3IP1, IFT20). This evidence concerns the gene IFT81 and ciliopathy.