They went searching for similar proteins in platelets, and found one, which they have named PAR4. Thrombin seems to be able to activate platelets by binding to PAR4 in mice, which explains the residual platelet activity in PAR3-deficient mice. It certainly seems as though PAR4 protein is found in human platelets too. We humans seem to use a dual signalling system based on PAR1 and PAR4. Coughlin suggests that it might have something to do with clotting being such an important defence system.
Redundancy allows for error and backup when things go wrong.
But he also proposes that maybe there can be other triggers for clotting than thrombin, which could also bind to the PAR4. Perhaps the two systems might allow slightly different clotting responses or different rates of clotting to different amounts of thrombin. For those designing drugs, the researchers suggest two lines of thought. They suggest that it might be necessary to block both receptor types for preventing thrombosis effectively. But alternatively, the second receptor might allow clever drug designs that prevent large-scale thrombosis, but allow specific clotting when there is damage to blood vessel walls, to prevent bleeding.