Th2 cells release inflammatory mediators and cytokines such as interleukins 4, 5, 9, 10, and 13 and Fas ligand that may contribute to the regulation of AAA progression, whereas Th1-derived interferon-gamma and CD40 ligand are associated with macrophage activation, regulation of vascular smooth muscle cell apoptosis, and aortic wall remodeling (2, 19–22). The gene discussed is CD40LG; the disease is triple-A syndrome.