In the development of tubular injury in DN, glucose was transferred into renal cells by facilitative transporters such as glucose transporter (GLUT)-1 and -4, and activated various cellular events and signaling pathways, including generation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), activation of the PKC and JAK-STAT pathways [23]. The gene discussed is SOAT1; the disease is liver dysplastic nodule.