Vaccinia virus moves around infected cells propelled by comet-like actin tails. Newsome et al. (see the Perspective by Hall) have uncovered an outside-in signaling mechanism, induced by extracellular vaccinia virus particles, that is ultimately responsible for stimulating actin-based motility of vaccinia virus by locally recruiting and activating Src at the plasma membrane. The highly localized signaling circuit explains why actin tails are only formed at the plasma membrane and strengthens the hypothesis that actin-based motility of vaccinia mimics receptor kinase signaling at the leading edge of migrating cells. The authors also found a role for Src in regulating a switch from microtubule-based to actin-based motility at the leading edge of cells.