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The considerable variation in patient sensitivity to warfarin is attributed in part to mutations in genes that govern metabolism of this anticoagulant agent and its target, vitamin K epoxide reductase (JW Oncol Hematol Apr 1 2008). One third of this variation in sensitivity arises from mutations in two genes: CYP2C9 (which encodes cytochrome P450:2C9) and VKORC1 (which encodes vitamin K epoxide reductase C1). Individuals with CYP2C9 mutations have diminished ability to metabolize warfarin, and those with VKORC1 group A haplotype have excess sensitivity to warfarin-induced inhibition. Heightened warfarin sensitivity is associated with greater difficulty in maintaining prothrombin times within the therapeutic range and with excess risk for bl…