After being phosphorylated, p38MAPK can induce the high expression of the downstream NF-κB signal pathway and, finally, promote the activation of inflammatory factors such as TNF-α, IL-1β, IL-6, and TGF-β1 and aggravate renal interstitial fibrosis and renal tissue inflammatory damage [35, 36], so inhibiting TGF-β1 may be the key of treating GN, as shown in Figure 11. The gene discussed is IL6; the disease is ganglioneuroma.