The role of experiments in heart development, the NRGs, ErbB2 and ErbB4 an important role in the development of the nervous system and the heart. NRG ErbB promote the proliferation of cardiomyocytes, hypertrophic growth inhibition of cardiomyocyte apoptosis and promote cell survival. GGF2 to promote embryonic rat neonatal rat cardiac myocytes DNA synthesis, and promote an increase in the number of myocardial cells. A net increase of the number of functional myocardial cells in the embryonic heart development process, related with the proliferation of myocardial cells, is still associated with myocardial cell survival. Study also observed that nearly 25% of the cells in serum-free matrix in primary cultures of neonatal rat cardiac myocytes number 4d died; contrary, a 30% increase in the number of cells added GGF2 GGF2 promote survival of cardiomyocytes in vitro . Expression the no function NRGs and ErbBs rats died of heart and nervous system abnormalities in the uterus. NRG1, ErbB2, ErbB3, ErbB4 is no function of the mutated gene experiments showed that embryonic mice, mutations in several other genes outside than ErbB3 and development 10. 5d, due to poor cardiac differentiation, lack of ventricular trabeculae and endocardial cushion while resulting in the death of the embryo. Hertig application NRG1 and insulin-like growth factor diffuses into the chambers of the heart found, NRG1 can promote the formation of trabecular ventricular wall, and insulin-like growth factor 1 had no effect. In addition, NRG1 and insulin-like growth factor 1 synergistically induced cardiomyocyte DNA synthesis, and promote the growth of the ventricular tight zone and AV cushion after two heart chamber development and maturation of the key. Prompt the NRG1 and insulin-like growth factor 1 interaction occurs affect the morphology of the heart chamber. Zhao et GGF2 with other pro-mitogen not identical, in serum-free low density alkylene fusion myocardial cell culture, GGF2 mechanism to promote the survival of neonatal and adult cardiomyocytes, in part is due to inhibition of apoptosis.