Moreover, growing evidence supports the role of different metabolic pathways and factors in the activation of inflammatory mechanisms involved in the pathophysiology of DN including the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, the nuclear transcription factor kappa B (NF-κB), the Rho-Kinase Signaling, and the nuclear factor erythroid 2-related factor 2 (Nrf2) (Figure 1). Here, SOAT1 is linked to liver dysplastic nodule.