Recent work highlights that diverse arrhythmogenic pathways may relate to specific desmosmomal proteins with PKP2 mutations/loss (CX43 hemichannel function, calcium handling, sodium channels) while other desmosomal proteins, such as DSP may impact classic CX43 channel functions, which may drive electrical dysfunction in the absence of structural disease in ARVC. The gene discussed is DSP; the disease is Arrhythmogenic right ventricular dysplasia.