Release of AGEs, production of reactive oxygen species (ROS), glycosylation of glomerular and tubular proteins with activation of Janus kinase/signal transducers/activators of transcription (JAK-STAT), nuclear factor-kB (NFkB), and p38 mitogen-activated protein kinase pathways are some of the hypothesized mechanism leading to DN and CKD secondary to DN. The gene discussed is SOAT1; the disease is liver dysplastic nodule.