EGFR and pancreatic neoplasm: Furthermore, lipopolysaccharide‐induced EGFR upregulation on macrophage surfaces is facilitated by Rab10, and inhibiting EGFR promotes M2 polarization via peroxisome proliferator‐activated receptor gamma (PPARγ)‐mediated glutamine metabolism, shifting the macrophage balance from M1 to M2.[365] A similar phenotype is observed in pancreatic cancer, where regenerating islet‐derived protein 4 (REG4) secreted by cancer cells activates the EGFR/AKT/cAMP response element‐binding protein (CREB) pathway in macrophages, promoting M2 polarization.[366]