Brugada syndrome, first described as a new clinical entity by Pedro and Josep Brugada in 1992, has attracted great interest because of its high prevalence in many regions of the world and its association with high risk for sudden death. The syndrome has captured the attention of the cardiac electrophysiology community because it serves as a paradigm for our understanding of the role of spatial dispersion of repolarization in the development of cardiac arrhythmias. The past decade has witnessed an exponential rise in the number of reported cases and a striking proliferation of papers serving to define the clinical, genetic, cellular, ionic and molecular aspects of this disease. This brief review summarizes the key clinical and experimental milestones that have brought us to our current understanding and approach to therapy of the Brugada syndrome.