In summary, mechanistic studies have revealed a remarkable capacity of F. nucleatum to remodel the CRC cell phenotype towards increased malignancy and stem-like features; this occurs via a diverse array of ligands, receptors, and molecular circuitries at the intersection of developmental (Wnt/β-catenin, Notch) and inflammatory (TLR/NLR, CARD3, NF-kB, NRF2) signaling networks. The gene discussed is NFKB1; the disease is colorectal carcinoma.