Due to reduced synthesis and increased thrombin cleavage, ADAMTS13 activity is impaired under inflammatory conditions facilitating the subsequent development of hyperactive vWF multimers.29In addition, vWF was shown to directly stimulate the proliferation of smooth muscle cells, a crucial component of arteriosclerotic lesions.30However, while vWF deficiency protects mice from atherosclerosis,30this protective effect has not been demonstrated in patients with von Willebrand disease.31Results from murine models must always be considered in the light that mice are not men. The gene discussed is VWF; the disease is Von Willebrand disease.