Further studies using other DCM models such as transgenic murine models lacking γ-sarcoglycan [45], dystrophin and MyoD [46], or animal models which have undergone transverse aortic constriction to induce DCM would be required to assess the potential therapeutic benefits of HMGB1 fragment for DCM patients. The gene discussed is HMGB1; the disease is familial dilated cardiomyopathy.