In order to answer these questions, we therefore developed a human model of CPVT2 derived from a patient carrying the G112+5X mutation in the CASQ2 gene through reprogramming to iPSCs, a technology that has served as a tool model for evaluating potential therapies for various cardiovascular diseases, including CPVT.9, 10, 25, 26 Similar to mouse models, AAV9-based administration of the human CASQ2 gene to CPVT2-CMs was sufficient to normalize the functional defect detected in those cells, demonstrating the therapeutic value of viral-based therapy of CPVT also in a human setting. This evidence concerns the gene CASQ2 and catecholaminergic polymorphic ventricular tachycardia.