Targeting ROS production with N-acetyl cysteine (72) or treatment with a S1PR3 antagonist (73) both reduces the proinflammatory polarization of Kupffer cells and is associated with less inflammatory liver damage, which suggests that the combination of these treatments might bring additional advantage to counteract pro-inflammatory skewing of intrahepatic macrophages due to hyperglycemia. The gene discussed is S1PR3; the disease is Hyperglycemia.