With their familiar snow-white coats sprinkled randomly with coal-black spots, Dalmatian coach hounds are one of the most distinctive of canine breeds. To students of purine metabolism, however, these animals are an intriguing “curiosity among mammalia,” not for their appearance, but for a dual defect in the transport of urate anions (1). In contrast to other dogs (and humans), most of the urate filtered by the glomeruli is not reabsorbed, tubular secretion continues, and uric acid excretion is therefore high. Concurrently, urate ions in plasma have limited access to the abundant uricase in hepatic cells, and allantoin production is thereby impaired. These defects roughly offset each other (Dalmatians excreting mainly uric acid and mongrels excreting mostly allantoin), such that plasma concentrations of urate are similar in all dogs. The Dalmatian differences in purine metabolism as well as the spots are transmitted in a classic Mendelian autosomalrecessive pattern, and all individuals of this breed are affected (2). Although all of this information is well established (3), recent advances in understanding cellular urate transport and in defining the canine genome make it appropriate to reexamine this unusual knockout of nature (4).