VSIG2 and pancreatic ductal adenocarcinoma: Functionally, VSIG2 behaves as a Janus-faced rheostat: in pancreatic ductal adenocarcinoma, VSIG2 partners with LAMTOR2 to hyperactivate mTOR, fuelling glycolytic reprogramming and aggressive invasion; conversely, in colorectal cancer, VSIG2 loss is linked to reduced M1 macrophage and B-cell infiltration, dampened antigen presentation, and shortened survival [8,9].