Mutated or dysfunctional ABCG2 may lead to significantly reduced excretion, moderate hyperuricemia and metabolic syndrome.139 Initially, it was hypothesized that the loss or reduction of ABCG2-mediated renal urate secretion would result in increased renal urate reabsorption, as diminished renal excretion is typically considered the primary mechanism of hyperuricemia in most gout patients. The gene discussed is ABCG2; the disease is hyperuricemia.