SLC16A3 and pancreatic ductal adenocarcinoma: In a prior study, the metabolic status induced by MCT4 was reported to be an important determinant of the immunosuppressive environment in pancreatic ductal adenocarcinoma.24 In another study, MCT4 was noted to functionally alter mitochondrial respiration and induce abnormal glutamine metabolism.34 Recent evidence suggests that MCT4 knockdown leads to enhanced intracellular accumulation of lactate and decreased glycolysis in LPS‐treated macrophages, which are essential to a vastly downregulated inflammatory response.35