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Biol Psychiatry (2019) 85:97106

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But the mechanism is receptor-mediated and tissue-specific, meaning KPV produces robust effects in conditions where MC1R signaling drives inflammation and produces minimal effects where other pathways dominate

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Moreover, other genetic traits, such as the functional deficiencies in cobalamin-dependent methionine synthase described above, could contribute to an increased relative risk of cardiovascular disease, but their respective contributions are not yet determined