demonstrated that BCAT2 deficiency inhibited tumor growth of pancreatic ductal adenocarcinoma (PDAC) by regulating lipid metabolism.[10] Although there were several researches documented that BCAT2 directly influenced the biological process of tumor by regulating metabolic related pathways, its role in regulating TME immune status has never been explored. Here, BCAT2 is linked to pancreatic ductal adenocarcinoma.