Qasim H, et al. - Researchers investigated the part played by Arhgef1 in platelet function using mice with a genetic deletion of Arhgef1 (ie, Arhgef1−/−) and determining platelet phenotype in these experimental models using a host of in vivo and in vitro platelet assays. Protracted carotid artery occlusion and tail bleeding times were seen in Arhgef1−/− mice. In comparison to wild-type littermates, defective aggregation, dense and α granule secretion, αIIbβ3 integrin activation, clot retraction and spreading were shown by the platelets derived from Arhgef1−/− mice. In addition, a defect in the activation of the RhoA–Rho-associated kinase axis, but not Rap1b, partly mediated the mechanism involved in the regulation of platelets by Arhgef1. Overall, a critical role of Arhgef1 in platelet function was shown, for the first time, in vitro and in vivo.