Besides increasing cancer cell “stemness,” F. nucleatum directly targets CR-CSCs via multiple interactions (CbpF/CEACAM1; Fap2-Gal/GalNac); F. nucleatum infection further increases the constitutively high Wnt activity of CSCs, while eliciting resistance to cell death and NF-kB- dependent chemokine release (see below 5.2) [68]. This evidence concerns the gene GAL and cancer.