Patient-specific iPSCs were differentiated into cardiomyocytes that were shown to be larger, with a highly structured and organized sarcomere and a preferential nuclear localization of NFATc4 (transcription factor associated with a calcineurin-mediated hypertrophic signaling, defined as nuclear factor of activated T cell 4), which is responsible for the hypertrophic phenotype seen in LS patient’s CMs compared to their healthy counterpart [124]. The gene discussed is NFATC4; the disease is Leigh syndrome.