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Disruption of <jats:italic>Kif3a<\/jats:italic>, a component of the Kinesin\u2010II motor complex, disables anterograde IFT and leads to failure in the formation and maintenance of cilia. Likewise, the absence of <jats:italic>IFT88\/Tg737\/Polaris<\/jats:italic>, a core component of the IFT particle, results in the loss of cilia. Although primary cilia were described on chondrocytes almost 40 years ago, only recently has the functional significance of IFT and cilia in skeletal development been uncovered through the use of mouse models containing mutations or deletions in genes required to make and maintain cilia. Together, the results indicate that primary cilia\/IFT are involved in coordinating multiple signaling pathways within the skeleton. 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