Research on the C-terminal of MUC16 in pancreatic cancer has shown a positive correlation with Foxp3 expression, aligning with serum CA125 levels and the proportion of circulating Tregs, where MUC16c’s activation of the IL-6 JAK2/STAT3 pathway enhances Foxp3 expression, thereby promoting Treg accumulation in tumor tissue (37). This evidence concerns the gene FOXP3 and pancreatic neoplasm.