The FeCl3-induced model of vascular injury and thrombosis in mice is now widely used to evaluate genetic and pharmacological interventions [24]. The two inbred strains had marked differences in the time for occlusion of the carotid artery after FeCl3 injury. After FeCl3 treatment, thrombus formation and occlusion was remarkably shortened in the A/J mice compared to the B6 mice. These results have not previously been reported. A recent study [25] of sheer stress in rats, found that the magnitude of changes in sheer stress with increased blood flow varied with the different strains. Further investigation, beyond the scope of this study would be necessary to determine the contribution in the differences in size and sheer stress of the carotids to arterial occlusion rates in the B6 and A/J mice. In preliminary studies, we have noted differences in the composition of the thrombus in B6 and A/J mice. The pattern of blood flow cessation for the two inbred strains was different than for the Lepob mice [26] with impaired platelet function, and coagulation time was similar in the two strains. In the mice with deficiencies of the Plg network [27], thrombus formation time was reduced in the Plg-/- mice, but increased in the PAI-/- mice, suggesting that alterations in plasmin activity that affect the rate of clot lysis, can modulate the events leading to occlusive thrombus formation.