Despite the wealth of information regarding extrinsic regulators of platelet function, considerably much less is known regarding the intrinsic mechanisms designed to avert excessively robust platelet activation after vascular injury. To that end, this research project investigates fundamental and mechanistic concerns regarding the biology, signaling and function of RGS16, in platelets. Results obtained from these studies may lay down the foundation for understanding, and developing novel agents and means for the therapeutic management of thrombosis-based disease states.