Familial cardiomyopathies, particularly those linked to the deletion of Arginine 14 in Phospholamban (PLN R14del), remain formidable challenges in medical genetics, often leading to arrhythmogenesis and sudden cardiac death. Traditional therapies have shown limited efficacy in treating these genetic anomalies. This study aims to utilize the prime editing system to efficiently introduce the PLN R14del mutation into human cell lines and iPSC-derived cardiomyocytes. The goal is to develop a methodology for correcting this mutation, ultimately aiming to prevent cardiomyopathy features in animal models. We employed a prime editing system to generate the PLN R14del mutation in a human cell line and iPSC-derived cardiomyocytes as a disease model. A series of pegRNAs, in conjunction with nicking gRNAs, were tested for efficiently installing the mutation. Subsequently, we applied similar methodologies to correct the R14del mutation in engineered HEK cells and patient-derived iPSCs harboring the mutation. The study progresses with the development of an Adeno-associated virus, with an optimal pegRNA, as a delivery vehicle for the translational approach. We successfully identified pegRNAs capable of installing and correcting the PLN R14del mutation without high indel rates. The ongoing research focuses on the efficacy of the prime editing approach in correcting the R14del mutation in humanized PLNR14del mouse and pig models, with the anticipation of preventing arrhythmogenic and dilated cardiomyopathy features. This research demonstrates prime editing's potential in treating familial cardiomyopathies, potentially leading to innovative therapies and foundational advances in genetic medicine.