We stand at the threshold of a new era in the understanding, diagnosis, and treatment of gout. During the past decade or so, our knowledge of the disease, and of uric acid biology in general, has advanced rapidly. Discoveries such as uric acid’s ability to activate the inflammasome [1], the loss of functional uricase along the evolutionary tree among the higher primates [2], and the putative role of uric acid as the “danger signal” [3] underline the ongoing relevance of uric acid biology. New drugs with old mechanisms of action have come to market (eg, febuxostat, a xanthine oxidase inhibitor) or may soon be arriving (eg, RDEA594 [Ardea Biosciences, San Diego, CA], a URAT1 inhibitor), and drugs with novel mechanisms for gout treatment have also received US Food and Drug Administration approval (pegylated uricase) or loom on the horizon (anti–interleukin [IL]-1 therapies). As we look to the future of gout therapeutics, it is important that we continue to improve on our use of old therapeutics even as we strive to embrace the new. Although long-available treatments for gout are (or had been) inexpensive and therefore accessible to almost all patients, they are often poorly utilized in the clinic, as exemplified by near-universal underdosing of allopurinol. As new drugs are introduced to the market, convincing physicians to optimize their use of older drugs becomes a more difficult proposition, especially in the face of marketing campaigns that promote the newer (and still on-patent) therapies.