Inflammatory response directly causes cellular toxicity, apoptosis, and necrosis through oxidative stress, and interplay of oxidative stress and inflammatory response leads to the activation of oxidative stress and the increased levels of pro-inflammatory mediators such as TNF-α [56] and interleukin-15 as an inflammatory cytokine independently associated with CAD and carotid intima-media thickness, suggesting a main role of IL-15 in the atherosclerosis process [57]. This evidence concerns the gene IL15 and coronary artery disorder.