An elegant study from this group which followed demonstrated that KO of luminal accessory protein TRDN (to mimic CPVT-linked loss-of TRDN-function mutations) causes profound changes in RyR2 complexes and subcellular structural organization, leading to almost 50% loss of contacts between T-tubules and junctional SR [17]. This evidence concerns the gene TRDN and catecholaminergic polymorphic ventricular tachycardia.