Therefore, we postulate that the primary effect of doxycycline is based on its inhibition of mitochondrial protein synthesis, preventing clonal expansion of T-cells and possibly also other proliferating cells in AAA tissue, thus, indirectly, resulting in a decrease of proinflammatory cytokines, MMP-2 and MMP-9 that otherwise damage the vascular stroma [9,28,41]. The gene discussed is MMP2; the disease is triple-A syndrome.