To investigate whether EIII-SNPs could induce a worsened phenotype of hemorrhage pathogenesis in vivo, following previously described methods [6,27], C57BL/6J mice were subjected to treatments of GST, EIII, SNPs, GST-SNPs, and EIII-SNPs for 24 h as first-hits, and then followed by 24 h treatment of antiplatelet (anti-CD41) antibody as second-hit. The gene discussed is ITGA2B; the disease is hemorrhage.