Many pathogens have evolved a variety of mechanisms to exploit the host-cell actin cytoskeleton during infection, either to enter into cells or to move within cells. These events have been investigated and documented in detail. Yet, a complete picture of the molecules and mechanisms regulating entry and intracellular movement remains to be established. Here we present a series of studies revealing that in addition to actin rearrangements the host cell also employs septins, a relatively newly characterized component of the cell cyto-skeleton, to regulate bacterial entry and restrict the dissemination of cytosolic bacteria. The challenge now is to decipher the precise role of septins during actin rearrangements and how these different cytoskeleton components orchestrate infection processes.