In order to clarify the molecular mechanism of congenital teratogenesis, establishment of an appropriate animal model for the investigation of the effects of exposure to environmental factors, the relationship between dosage and external malformations, as well as visceral, is essential.Historically, knowledge of the embryogenesis of any cardiovascular defects has been difficult to attain because of the lack of models in which the pathogenesis of the defects could prospectively be studied.We focused on embryonic deaths, external malformations, and visceral malformations of cardiovascular origin caused by maternal exposure to ^{60</SUP<Co gamma rays and excess Tretinoin. Following maternal exposure to Tretinoin, we observed a high incidence of 100% teratogenesis, especially cardiovascular conotruncal defects and craniofacial anomalies, such as transposition of the great arteries, dextroposition of aorta, riding aorta and aortic arch anomalies including interruption of aortic arch and aortic coarctation, along with craniofacial anomalies were micrognathia and a cleft palate. These results indicate the high Tretinoin sensitivity of mouse fetuses to conotruncal anomalies and neurocristopathy syndromes. In humans, these conditions are termed DiGeorge-Velocardiofacial Syndromes.The Tretinoin treatment of mice could be a suitable animal model to study the mechanism of human complex congenital abnormalities including cardiovascular and craniofacial anomalies, especially DiGeorge-Velocardiofacial Syndromes.}