We conclude that these mutually supportive data reinforce the hypothesis that fluvastatin decreases the endothelial capacity for plasma VWF and platelet recruitment, significantly diminishing its potential prohemostatic capacity and effectively countering at least these parameters caused by the loss of a normal level of ADAMTS‐13 function as observed in the plasma of patients with TTP. The gene discussed is VWF; the disease is thrombotic thrombocytopenic purpura.