These representative case reports also show that depending on the severity of the disruption of the urate transportability of ABCG2, homo- or heterozygosity of the dysfunctional polymorphisms and further genetic predispositions in other genes involved in urate homeostasis [106], hyperuricemia can already occur in childhood (pediatric-onset), which increases the risk for the development of early-onset gout. The gene discussed is ABCG2; the disease is hyperuricemia.