In atherosclerosis, circulating monocytes are recruited to atherosclerotic lesions where they activate to become macrophages and engulf oxidized low‐density lipoprotein (oxLDL), transforming into foam cells that secrete cytokines (e.g., IL‐1β, TNF‐α) and matrix metalloproteinases (MMPs), promoting inflammation, plaque instability, and potential rupture [74]. This evidence concerns the gene IL1B and atherosclerosis.