Brugada syndrome is a heterogeneous genetic channelopathy that predisposes to ventricular arrhythmias and sudden cardiac death (SCD). The electrocardiogram (ECG) fi ndings only suggest a diagnosis of Brugada syndrome but are not confi rmatory. The ECG pattern is known to vary with time in some patients and many have a normal baseline ECG [1,2]. There are two distinctly described ECG patterns, type I Brugada is characterized by ST elevation (≥2mm) with a "coved" pattern or a T-wave which is inverted with an upward convexity, in other cases the elevated ST segment descends and rises again forming a "saddleback" type pattern, this is called the type II Brugada. The electrophysiological and clinical manifestations of this syndrome have been found to be secondary to various factors [3][4][5][6][7][8][9][10]. Of these, mutations in cardiac sodium channel SCN genes (SCN5A and SCN10A) are the most well-known [11]. Since all affected families do not have these mutations, it is believed that other mutations in sodium channel genes or mutations in non-sodium channel genes may also cause Brugada syndrome [12][13][14][15].There have been some cases with a normal baseline EKG where in a Brugada pattern was induced by factors such fever, infection, cocaine use and even medication, particularly sodium channel blocking agents. With SCD being a common presenting symptom, it is critical to make an early diagnosis and institute preventive treatment such as an implantable cardioverter defi brillator. Our case described below is of a patient who presented to the emergency room (ER) with a fever and was found to have a pattern of ST elevation without any other cardiac symptoms.The patient is a 71 year old male who presented to the emergency room with fever (103.5 F). An ER ECG ( Figure 1) showed RBBB, coved ST elevation in leads V1-V4 with T-inversion characteristic of Type I Brugada syndrome. He was urgently taken for left heart catheterization, which revealed normal coronaries. An echocardiogram performed two days after this showed normal left and right ventricular function.His EKG went back to his baseline pattern of RBBB/LAFB after fever resolution (Figure 2) and a diagnosis of type I Brugada syndrome unmasked in the setting of fever was made. He was offered defi brillator implantation, but he opted for conservative management.Upon asking for a prior history of syncope, he reported two events; one when he was seventeen and another in his thirties.Both times he was in a hot environment and experienced a prodrome of feeling confi ned and crowded before briefl y losing consciousness, suggestive of a vasovagal etiology and did not seek medical attention at the time.Brugada syndrome triggered by fever is known to predispose to malignant ventricular arrhythmias. Other factors