Brugada syndrome has been linked to mutations in genes coding sodium and calcium transporters, notably SCN5A, CACNA1C, and CACN2b [8,9]. Cases of acquired Brugada syndrome in the setting of antiarrhythmic sodium and calcium channel blockers are well described and represent the basis for drug provocation tests used to assess individual risk for and prognosis of Brugada syndrome. The gene discussed is CACNA1C; the disease is Brugada syndrome.