Gout is a common metabolic disorder characterized by elevated uric acid leading to the formation and accumulation of uric acid crystals in synovial fluids. An attack of gout is characterized by intense, self-limited bouts of acute arthritis with excruciating pain. The mechanisms regulating initiation and resolution of gouty inflammation are still unclear. A significant though incomplete body of information implicating the innate immune system as a central component of immune and inflammatory cell activation in gout has been accumulated over the past few years. In this review, advances in the understanding of the basic biology of crystal-mediated inflammation are summarized. The emerging role of the inflammasome and the cytokine interleukin-1 in the initiation of acute gout is highlighted. How these findings may open a door to a new approach for therapy with the development of interleukin-1 antagonists is discussed.