Over the years, the pathophysiological mechanisms of DN have been intensely investigated and are currently recognized to be multifactorial, with derangements in metabolism, hemodynamics, inflammation, and autophagy, leading to dysregulated signaling cascades including Janus kinase/signal transducer and activators of transcription (JAK/STAT), protein kinase C, and nuclear factor-κB (NF-κB)3. The gene discussed is SOAT1; the disease is liver dysplastic nodule.