SOD2 and neoplasm: Furthermore, the oral administration of Clostridium butyricum in orthotopic mouse models of PDAC led to increased tumor colonization by C. butyricum and decreased tumor weight, while the primary metabolite of C. butyricum, butyrate, drove the accumulation of ROS, lipid droplets and triglycerides along with the downregulation of superoxide dismutase 2 in a pancreatic cancer cell line, ultimately inflicting metabolic disruption and cell death of the cancer cells and thus providing a putative mechanism of how C. butyricum acts in the pancreatic TME to promote tumor regression [107].