TIGIT and neoplasm: Developing small-molecule inhibitors or monoclonal antibodies that block the interaction of FadA with E-cadherin or Fap2 with its receptors (Gal-GalNAc on tumor cells or TIGIT on immune cells) could disrupt bacterial colonization and dismantle its immunosuppressive shield without killing the bacterium, thus posing a lower risk of inducing resistance [102].