Many pathogenic mechanisms have been proposed such as direct invasion of the vascular endothelial wall by pathogens and the instigation of focal inflammation, acceleration of atherosclerosis through induction of proinflammatory cytokines (such as TNF-alpha, interleukin 2) in response to specific antigenic stimuli, infection-induced cardiac arrhythmias and infectious burden due to chronic infections which may dysregulate the magnitude of immune responses [130]. This evidence concerns the gene IL2 and atherosclerosis.