Chemotaxis, the process by which cells can detect and migrate up a chemottractant gradient, is widespread and is of wide biological importance. Neutrophils and other inflammatory cells enter sites of infection and inflammation in response to a shallow gradient of chemoattractants. Chemotaxis is mediated by trimeric G-protein–coupled receptors, which trigger complex signaling responses that regulate the reorganization of the actin cytoskeleton that underlies cell motility. Newly synthesized actin polymers at the leading edge (the pseudopod) protrude in the forward direction, while myosin-based contraction of the trailing edge facilitates substrate de-adhesion, resulting in forward propulsion. In the 25 July Cell, Jingsong Xu and colleagues at the University of California, San Francisco, investigate neutrophil motility and propose a model explaining how cytoskeletal assemblies modulate cell sensitivity to attractants (Cell, 114:201-214, July 25, 2003).