These include transfer of periodontal bacteria to atheromatous plaques, change of lipid metabolism, endothelial dysfunction, shared genetic risk factors and, focusing on LGI, the spillover in the bloodstream of proinflammatory cytokines from periodontal tissues, in particular IL-6 and TNF- α, which have been found augmented in periodontal patients. The gene discussed is IL6; the disease is endothelial dysfunction.