Primary cilia are antenna-like cellular organelles that act as sensory receptors and also play an important role in signal transduction. Formation of these structures occurs as cells exit the cell cycle, whereupon centrioles migrate to the apical domain and become the basal bodies that anchor the new cilia as it forms. Centrosomal protein CP110 is a crucial regulator of centriolar division during the cell cycle and is thought to act as a key suppressor of ciliogenesis, based on in vitro studies. In this issue (p. 1491), Anand Swaroop and colleagues add a new twist to this theory and show that, in vivo, the absence of CP110 results in a failure to make cilia in a Cp110−/− mouse model. The authors show that ablation of Cp110 causes lethality shortly after birth due to organogenesis defects that are similar to those observed in ciliopathies. Using serum-starved embryonic fibroblasts derived from Cp110−/− mice, they further demonstrate a failure of basal body docking to membranes during cilia formation. These data challenge the prevailing view and demonstrate a more complex role of CP110 in the ciliogenic pathway, and highlight the importance of in vivo studies for our understanding of ciliogenesis in a physiologically relevant setting.