Hypomorphic fibrillin-deficient mice as an animal model of Marfan syndrome which develop spontaneous aortic dilatation and aneurysms of the ascending aorta by three months of age showed increased IL-6 transcription and secretion in aortic tissue at the end of the study at three months, accompanied by increase in secretion of monocyte chemotactic protein-1 (MCP-1) and GM-CSF,[4]. The gene discussed is IL6; the disease is Marfan syndrome.