Loss-of-function variants have been associated with elevated TGFβ signaling and myocardial fibrosis in SCN5a-deficient mice, supporting a role for sodium current reduction in TGFβ-mediated structural remodeling through enhanced fibroblast activation, extracellular matrix deposition, and myocardial scarring [41, 42]. This evidence concerns the gene SCN5A and Myocardial fibrosis.