Inflammatory cells such as monocytes/macrophages, neutrophils, T cells (different subsets including Th1, Th2 and NKT cells), B cells, mast cells and NK cells infiltrate the vessel wall and locally secrete cytokines, chemokines and other inflammatory factors resulting in the progression of AAA.[3, 10] CD4+ T cells dominate these infiltrates,[14] but it is still unclear which T cell subclass is responsible for the pathology of AAA. The gene discussed is CD4; the disease is triple-A syndrome.