In contrast, HDAC4 (a master negative regulator of cardiac hypertrophy) was found to repress the activities of MEF2 and serum response factor (SRF) under physiological conditions, but in cardiac hypertrophy became oxidized, causing it to shuttle out of the nucleus and allow de-repression of pro-hypertrophy genes [47]. The gene discussed is SRF; the disease is cardiac hypertrophy.