Many acute thrombotic complications of atherosclerosis result from the fracture of the plaque’s fibrous cap.[1] Proteolytic activity within the atheroma favors degradation of extracellular matrix macromolecules that lend tensile strength to the plaque’s fibrous cap.[2, 3] Interleukin-1 (IL-1), a cytokine implicated in vascular inflammation,[4, 5] induces the expression by cells found in atheromata of several matrix-degrading proteases implicated in lesion remodeling.[6–8]. The gene discussed is IL1A; the disease is atherosclerosis.