Toxoplasma gondii, the protozoan parasite that causes toxoplasmosis, initiates invasion of its host cells by inducing the assembly of a parasite–cell junction. Concomitantly, the plasma membrane of the host cell invaginates around the parasite to form a parasitophorous vacuole (PV). The parasite then propels itself through the junction and multiplies in its host cell within the PV. Given the size of the parasite, PV formation and parasite internalization are likely to require local loosening of the host cell cortical actin barrier, but how is this achieved? On page 4333, Isabelle Tardieux, colleagues and collaborators propose that toxofilin, an actin binding protein secreted by T. gondii, facilitates parasite invasion by regulating host cortical actin filament turnover. They show that parasites lacking toxofilin are impaired in cell invasion, although they eventually enter host cells, and that toxofilin secreted by invading parasites specifically associates with areas of host cell actin meshwork disassembly. Finally, quantitative fluorescent speckle microscopy indicates that toxofilin expression accelerates actin filament turnover in epithelial cells. Together, these data suggest that toxofilin upregulates actin turnover at parasite entry points, thereby locally loosening the host cell actin meshwork and facilitating parasite invasion.