In both LN patients and animal models, miR-155 is significantly upregulated and positively correlates with disease activity.SOCS1 is an important negative feedback regulator in the JAK/STAT signaling pathway, modulating inflammatory responses by inhibiting JAK1 activity and regulating STAT1 phosphorylation (199).Studies have shown that miR-155 promotes inflammatory signaling by downregulating SOCS1, thereby relieving its inhibition of the JAK1/STAT1 pathway, which enhances M1 macrophage polarization and indirectly exacerbates podocyte injury. The gene discussed is SOCS1; the disease is lobular neoplasia.