After Hasegawa et al. first proposed in 1991 that tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) were involved in the pathogenesis of DN [2], more and more epidemiological and preclinical findings have since suggested that systemic and local renal inflammation plays a key role in the development and progression of DN. The gene discussed is IL1B; the disease is liver dysplastic nodule.