The invasive pathogen Salmonella enterica has evolved sophisticated mechanisms to subvert the cytoskeletal machinery of its host. Following contact with the host cell, it delivers a distinct arsenal of effector proteins directly into the cytoplasm. These bacterial effectors coordinate transient actin rearrangements and alter vesicle trafficking to trigger invasion, without causing overt cellular damage. Recent studies have shed new light on the signaling mechanisms underlying this remarkable host-pathogen interface, in particular, highlighting the unique multi-functional role and temporal regulation of key bacterial effectors.