P. gingivalis contributes to endothelial dysfunction, chronic inflammation, and atherogenesis by activating Toll-like receptors (TLR2 and TLR4), upregulating the NF-κB signaling pathway, and inducing the production of key pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). This evidence concerns the gene NFKB1 and endothelial dysfunction.