In preclinical models of gene therapy involving AAV9 and CRISPR/cas9 strategies, disruption of the PLN-R14del mutation (which leads to abnormal PLN protein) has shown potential to prevent impairment of the sarcoplasmic and/or endoplasmic reticulum Ca2+-adenosine triphosphatase 2a activity, reduce disruption of Ca2+-handling, and attenuate ARVC pathogenesis180,181 (Table 2). The gene discussed is PLN; the disease is Arrhythmogenic right ventricular dysplasia.