During DN, the increased expression of JAK in glomerular podocytes aggravates the persistent inflammatory response of the kidney by activating the STAT3/NF-κB pathway.52,53 In DFU, the increasing expression of IL-6 results in a sharp increase in phosphorylated STAT3 levels,54 which mediates impaired immune cell activation, recruitment, and survival, resulting in delayed wound healing.55 The gene discussed is STAT3; the disease is liver dysplastic nodule.