Taking Vesicular Transport to the Cilium

Defects in protein trafficking within the cell body and cilia are thought to underlie the human disease Bardet-Biedl syndrome (BBS). In this issue, reveal that a large complex of proteins implicated in BBS cooperates with Rabin8—the GTP exchange factor for the small GTPase Rab8—to promote cilia formation and presumably movement of membrane proteins from the cell into the cilium.