The ability of cells to migrate is central to many developmental processes and is important for the understanding of cancer progression. Cell motility is the result of actin polymerisation at the leading edge of cell protrusions, which is mediated by the wave regulatory complex (WRC). An important factor in vesicle trafficking, the exocyst complex, mediates polarised exocytosis and has been proposed to be involved in the positioning of actin regulators to the leading edge in migrating cells. In this issue (p. 3756), Maria Carla Parrini and co-workers report a direct connection between WRC and exocyst in the context of cell motility. They find that the exocyst complex subunits Exo70 and Sec6 interact with the WRC members Abi1 and Cyfip1 both in vitro and in human cells. Importantly, this interaction occurs independently of the shared interactor of WRC and Exo70, the Arp 2/3 complex, which is a main regulator of the actin cytoskeleton. The association between the WRC and exocyst complex contributes to cell migration, as Exo70 truncations, which prevent the binding to WRC, inhibit cell motility. The authors also identify a forward flow of the WRC complex to the front edge in nascent protrusions and describe a correlation between WRC recruitment and the velocity of edge movements at the protrusion sites. Because both velocity and optimal WRC recruitment require the exocyst complex, this work clearly establishes a link between the actin polymerization machinery and exocytosis in the stimulation of cell motility.