In periodontitis, lipopolysaccharide from Porphyromonas gingivalis, a key pathogen, activates NF-κB through the TLR4/MyD88/NF-κB pathway, and causes nuclear translocation of NF-κB, induces the upregulation of MyD88 and NF-κB gene expression [50]. This evidence concerns the gene NFKB1 and periodontitis.