The authors suggested that the similarity between electron dense deposits observed in cardiomyocytes of EA patients and skeletal muscle myopathies occurring in patients harboring mutations in genes encoding α‐actin, nebulin, and titin might link EA pathogenicity to a sarcomeric protein, or perhaps to a transcription factor required to maintain the expression of sarcomeric genes. The gene discussed is TTN; the disease is Esophageal atresia.