Studies in Scn3b−/− mice revealed spontaneous cardiac arrhythmia and conduction abnormalities [14] and the recently uncovered structure of trimeric β3 subunits of Na+-channels together with their suggested interactions with α subunits [27] predict future testing of β subunit dependent μ-conotoxin sensitivity of Na+-channels [47] in disease or treatment. This evidence concerns the gene SCN3B and cardiac arrhythmia.