EGR1 and cardiac hypertrophy: NAB1 is highly expressed in cardiac myocytes and regulates cardiomyocyte growth through interaction with EGRs.[12] Transgenic mice expressing NAB1 displays an ability to inhibit pathological cardiac growth by repressing EGR activity in vivo.[12] Overexpression of NAB1 and deletion of EGR1 have been shown to protect the heart from pathological cardiac hypertrophy and fibrosis.[12] Interestingly, overexpression of NAB1 does not influence physiological cardiac growth response.