TIGIT and colorectal carcinoma: Fap2 recognition of Gal-GalNAc motifs in dysplastic epithelium and TIGIT engagement on NK/T cells explains the selective enrichment of the bacterium in CRC and its contribution to immune escape [115], in line with the NLRP3-driven, prostaglandin-rich microenvironment that promotes epithelial proliferation and oxidative DNA damage [116].