Neuromuscular injuries typically disconnect motor nerves from the muscles they innervate. Recovery requires reestablishing these connections, which often occurs outside of the central nervous system (e.g., in an arm). This capacity for functional regeneration is all the more impressive when one considers that, in an analogy of scale, the growing tip of the axon is able to find a spot the size of a dime in the middle of a football field, stop precisely on that dime, and "dance" (form a new synapse). However, in the case of injury to the muscle, reinnervation can be impaired by disintegration of the original muscle's synaptic site (or loss of the "dime"). Researchers therefore seek a molecular understanding of what cues muscles employ to control synapse formation by motor nerves. CROET's Dr. Bruce Patton identified a muscle surface protein that contains two components not present in the rest of the muscle, and mice were genetically engineered to lack these components. In the first mutant strain, synapses formed correctly during muscle development in embryos but, after injury in adults, motor nerves were not able to reinnervate synaptic sites in the muscle. In the second strain, synapses were unable to form correctly even in development, leading to an inability to survive after birth. Together, these discoveries pinpoint an essential biochemical signal normally used by muscle to promote its innervation. This information will guide efforts to improve recovery from neuromuscular injury and disease, perhaps by leading to molecular treatments to improve recovery following nerve and muscle injury.