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The effects of genetic polymorphisms on the rates of drug metabolism are well known, but how these polymorphisms influence the susceptibility to drug-drug interactions is less clear, in particular considering warfarin-drug interactions, whether reduced function proteins (e.g., CYP2C9*3 ) are inhibited to the same extent in vivo as wild-type proteins (e.g., CYP2C9*1 )

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Hence, increased DA signaling might contribute to mPFC hyperexcitability as reported here and previously reported hyperactive DA neurons in the ventral tegmental area [4, 5]

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