Both SLE and RA are now recognized as independent risk factors for atherosclerosis, where disease mechanisms involve pro-inflammatory cytokines (e.g., tumor necrosis factor (TNF)-α, interleukin (IL)-6, type 1 interferons), oxidative stress, and endothelial dysfunction, which in turn lead to fibrosis of the vasculature and proliferation of smooth muscle cells [26,27,28,29,30,31]. Here, IL6 is linked to endothelial dysfunction.