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The pathophysiological mechanisms of BrS were studied in different models, including animal models, heterologous expression systems, and human\u2010induced pluripotent stem cell\u2013derived cardiomyocyte models. Currently, only a few BrS studies have used human\u2010induced pluripotent stem cell\u2013derived cardiomyocytes, most of which have focused on genotype\u2013phenotype correlations and drug screening. The combination of new technologies, such as clustered regularly interspaced short palindromic repeats (CRISPR)\/Cas9 (CRISPR associated protein 9)\u2010mediated genome editing and 3\u2010dimensional engineered heart tissues, has provided novel insights into the pathophysiological mechanisms of the disease and could offer opportunities to improve the diagnosis and treatment of patients with BrS. 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