Inflammation (mediated in part by an increase in levels of the serum C-Reactive Protein and inflammatory cytokines tumor necrosis factor-α [TNF-α], interleukin-1 [IL-1], and IL-6), oxidative stress, and endothelial dysfunction have been proposed as the underlying mechanisms for the interrelationship between periodontitis and these diseases22–27. The gene discussed is IL1B; the disease is periodontitis.