The significant physiological role of p300 in postnatal cardiac structure and function is supported by the finding that transgenic mice with p300 lacking the cysteine/histidine rich zinc binding domain 3 (C/H3) (p300CH3ΔTG) die by ~20 weeks of age due to cardiomyopathy-associated cardiac dysfunction, including significantly decreased fractional shortening, ejection fraction, left ventricular systolic pressure, and left ventricular end diastolic pressure [35]. This evidence concerns the gene EP300 and cardiomyopathy.