The role of F. nucleatum in CRC pathogenesis has not been comprehensively understood, but at least four mechanisms have been suggested to describe the same28: (1) cell proliferation through Wnt signaling by an interaction between FadA and E-cadherin, (2) antitumor immune evasion via Fap2 and T cell immunoreceptors having Ig and immunoreceptor tyrosine-based inhibitory motif domains, (3) tumor binding and enrichment of Fap2 and Gal-GalNAc, and (4) chemoresistance by lipopolysaccharide and Toll-like receptor 4. This evidence concerns the gene CDH1 and neoplasm.