Although not unexpected – since MYH6 is more abundantly expressed in atria than in ventricles – these findings demonstrate the feasibility of using HLHS-derived iPSC-cardiomyocytes as in vitro tools to test drugs that target atrial contractility to alleviate HLHS deficiencies, or to design strategies that alter developmental pathways in order to minimize or even prevent development of MYH6-variant-associated HLHS. This evidence concerns the gene MYH6 and hypoplastic left heart syndrome.