Several studies using mouse models of atherosclerosis and acute coronary syndrome have shown that the increased expression of miR-9 contributes to a reduction in the aortic plaque area, collagen fiber proliferation, macrophage levels, and inflammatory cytokines IL-6, IL-1β, and tumor necrosis factor-α (TNF-α) by suppressing syndecan-2 (SDC2), the FAK/ERK signaling pathway, and p38-mitogen-activated protein kinase (p38MAPK), thereby reducing atherosclerosis processes [20,21]. This evidence concerns the gene IL1B and atherosclerosis.