GSK3β is also implicated as its pharmacological inhibition prevents and reverses the ARVC phenotype (including arrhythmias, contractile dysfunction, myocyte injury, apoptosis, exercise-induced sudden cardiac death (SCD), and redistribution of junctional proteins) in ARVC models in vitro, in vivo, and ex vivo including transgenic zebrafish and mouse models with cardiac-specific expression of the JUP2157del2 variant.23 This evidence concerns the gene GSK3B and Arrhythmogenic right ventricular dysplasia.