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. The gene discussed is CTLA4; the disease is familial pancreatic carcinoma.