The platelet integrin α_IIbβ₃ resides in a low-affinity state that transitions to a high-affinity state for ligand binding upon platelet activation. This transition is mediated by inside-out signaling. Once bound by a ligand, such as fibrinogen, outside-in pathways are triggered to support more platelet changes, such as spreading and clot retraction. The work by Pang et al demonstrates outside-in signaling is facilitated by shear forces on the integrin mediated by an intracellular G protein that ultimately increases the procoagulant potential of the platelet. PS, phosphatidylserine.