Accordingly, either the absence or poor CD226 expression on T cells can favor the engagement of CD155 with TIGIT, thus impairing T cell mediated anti-tumor response through different mechanisms: (i) inhibition of the AKT-mTORC1 pathway, with stabilization of FOXP3 and preservation of Treg immunosuppressive function [198] and (ii) recruitment of Src Homology 2-containing Inositol Phosphatase 1 (SHIP1) [199]. The gene discussed is CD226; the disease is neoplasm.