Similarly, cardiac-specific deletion of HDAC2 has also no adverse effect on heart development or function, whereas cardiac-specific knockout of both, HDAC1 and HDAC2 together, results in severe cardiac defects including dilated cardiomyopathy and arrhythmias and thereby neonatal lethality [11], implying functional redundancy of HDAC1 and HDAC2 in mammals. The gene discussed is HDAC2; the disease is dilated cardiomyopathy.