The ECG manifestations of BrS are often dynamic or concealed and may be unmasked or modulated by sodium-channel blockers, a febrile state, vagotonic agents, high vagal tone (large meals, during rest, or while sleeping), α-adrenergic agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. Other variations are frequently seen in the ECG of Brugada syndrome, such as prolonged P-wave, PR interval, or QRS duration, particularly in patients with an SCN5A mutation. This evidence concerns the gene SCN5A and hypercalcemia disease.