Many of the available inbred mouse strains, such as C57BL/6J (B6) and A/J, have been classified as resistant or susceptible to particular complex diseases (Table 1). These two strains have diverse responses to diet-induced obesity [8] (B6 susceptible; A/J resistant), diet-induced atherosclerosis (B6 susceptible; A/J resistant) [9], arterial ligation-induced neointimal hyperplasia (B6 resistant; A/J resistant), and ligation induced vessel remodeling (B6 resistant; A/J susceptible) [10]. These conditions are predisposing to thrombosis per se, but these mice have not been systematically evaluated for thrombosis. Clot formation and lysis, which ultimately determine thrombosis, requires platelet aggregation, coagulation, and fibrinolytic functions. Interactions among these pathways may occur and additional factors may modulate these processes. Identification of novel modulators and factors of these pathways can be identified by associating the phenotype with a location(s) on a specific chromosome, a quantitative trait locus (QTL).