SCN5A and Brugada syndrome: Monogenic murine cardiac models successfully demonstrated clinically observed atrial and ventricular arrhythmic phenotypes and their mechanisms following loss of Scn5a function replicating Brugada Syndrome and following challenge by class I, Na+ channel blocking drugs, both situations compromising AP conduction (Dautova et al., 2010, Guzadhur et al., 2013, Martin et al., 2012).