Clinical case studies have shown that p-STAT3 protein expression is significantly elevated in renal tissues of HBV-GN patients, and HBx activation of the JAK2/STAT3 signalling pathway upregulates the Bax/Bcl-2 ratio, which may be related to the pathogenic mechanism of HBV-induced nephritic tissue damage (He et al., 2013). The gene discussed is BCL2; the disease is ganglioneuroma.