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Understanding how the culprit mutant proteins alter normal heart function could lead to more effective treatments. One candidate is the giant protein tintin, which is mutated in a subset of patients with dilated cardiomyopathy. Through a combination of patient-derived stem cells, tissue engineering, and gene editing, Hinson\n            <jats:italic>et al.<\/jats:italic>\n            found that disease-associated titin mutations disrupt the function of the contractile unit in heart muscle. 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