Proarrhythmic reductions in conduction velocity have been attributed to compromised cardiac Na+ channel function in genetically modified Scn5a+/− murine models modelling the Brugada Syndrome (Huang, 2017; Kalin, Usher‐Smith, Jones, Huang, & Sabir, 2010; Martin, Grace, & Huang, 2011; Martin, Guzadhur, Grace, Lei, & Huang, 2011; Sabir, Killeen, Grace, & Huang, 2008). This evidence concerns the gene SCN5A and Brugada syndrome.