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Missense mutations account for most of type 2 vWD, whereas major disruptions in the vWF gene produce type 3 variants. The molecular basis of type 1 vWD is largely undefined. The laboratory diagnosis of vWD and its several variants is made on the basis of immunologic and functional studies of vWF, factor VIII levels, and specialized electrophoretic analyses (multimer gels). The mainstay of therapy for most patients with vWD is desmopressin, a pharmacologic agent that stimulates the release of endogenous pools of vWF. 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