The latter causes tumor growth stimulation, e.g., through the interaction of the adhesin FadA to E-cadherin and subsequent activation of β-catenin translocation to the nucleus11,32, or by interaction with the T-cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT) on T cells or natural killer (NK) cells via the adhesin Fap233. This evidence concerns the gene CDH1 and neoplasm.