Distinctive expression of immune checkpoint molecules, including PD‐1, TIGIT, GITR and CTLA‐4, has been found in Treg cells, which manifests different phenotype and subtype of Treg cells in TME.[36] In our study, MET activation specifically promotes GITR+ Tregs accumulation, a subset known for heightened suppressive activity.[25] High levels of GITR+ Tregs are linked to poor prognosis in pancreatic cancer, suggesting that MET signaling could promote immunosuppression within the TME by reprogramming intratumoral Tregs evolution. This evidence concerns the gene TIGIT and familial pancreatic carcinoma.