As insulin suppresses pro-inflammatory transcription factors, such as nuclear factor-κβ (NF-κβ), and also suppresses reactive oxygen species (ROS) generation, insulin resistance therefore also has a comprehensive pro-inflammatory effect (Fig. 1, pathways: 3c-18-FFA-37-plasma lipids-34-12- LDL-33-oxLDL-51-hypercholesterolaemia). The gene discussed is INS; the disease is Insulin resistance.