First, it is important to highlight the fact that few studies have suggested a potential role of rare TTN variants as phenotypic modifiers in BrS, LQTS, as well as sudden arrhythmogenic death syndrome (SADS) and sudden unexplained arrhythmogenic syndrome (SUDS) [25,26,27], but no definite causative association to any inherited channelopathy is widely accepted to date. The gene discussed is TTN; the disease is channelopathy.