Hernandez KR, et al. - Researchers used a genetic knockout mouse model method and a number of in vitro and in vivo assays to assess the role(s) of regulator of G-protein signaling (RGS) in platelet function, activation and thrombus formation. Compared to wild type (Rgs16^+/+) littermates, platelets from the RGS16 knockout (Rgs16^−/−) mice exhibited much more obvious agonist-induced platelet aggregation, secretion, and integrin activation. Also, compared with the controls, a significantly shortened bleeding time was seen in the Rgs16^−/−mice and they were more susceptible to vascular injury–associated thrombus formation. Overall, based on the findings, RGS16 was suggested to be an important regulator of hemostatic and thrombotic functions of platelets in mice, and therefore, constitutes a potential therapeutic target for modulating platelet function.