Altered protein activity and imbalance in MMP10-TIMP1 homeostasis by gene polymorphism may underlie the pathogenesis of atherosclerosis through increased destruction of ECM, activation of further MMPs and vascular smooth muscle cells (VSMCs), modified macrophage adhesion and migration, modulation of inflammatory responses with increased cytokine and chemokine activity, and thinning of the fibrous cap12–15. This evidence concerns the gene MMP10 and atherosclerosis.