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SCN5A inhibits BrS. 2 / 2
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"This might point to the fact that loss-of-function mutations in SCN5A and GPD1L might not be sufficient to cause BrS but could act like a revelatory factor such as a sodium channel blocker challenge."

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"In such cases, cardiac fibrosis contributes to the pathogenesis in varying degrees.Diffuse ventricular myocardial fibrosis in the right ventricular outflow tract was observed in patients with BrS.4 12 The missense mutation S910L was previously reported by Kapplinger and colleagues9 in a case of BrS, which was caused by the loss of function of SCN5A."