Damage-associated molecular patterns released from necrotic myocardium activate the immune system, recruiting inflammatory cells, including macrophages, neutrophils, and T lymphocytes, to both affected and non-culprit coronary arteries.[20] Macrophages, while clearing debris from ruptured plaques, produce pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), promoting inflammation and atherosclerosis progression in NCVs.[21–23]. This evidence concerns the gene IL1B and atherosclerosis.