As a way of enhancing infections, bacterial pathogens often alter host cell signaling pathways. Here, we describe recent work that highlights a new phosphatase from an intestinal and wound-invading pathogen that manipulates host cell phosphoinositide circuits. Despite the active-site homology between bacterial inositol phosphatases and mammalian phosphatases, sequence diffierences between them suggest that the development of speci?? c inhibitors may be feasible.