TIGIT and neoplasm: nucleatum may even provide a growth advantage for the tumor, due to the bacteria’s ability to inhibit NK cell-mediated tumor cell death via binding of the bacterial protein Fap2 to one of the NK cell inhibitory receptors, TIGIT.50 The procarcinogenic capability of F. nucleatum in the gut may be highly strain-dependent, as some strains have been resistant to colonization in mouse gut and required daily inoculation47 while others have been found to colonize readily.49