Since previous studies on other chronic kidney diseases have demonstrated that JAK2 is overexpressed in diabetic renal diseases (33) and that podocyte loss is induced by type I IFN in viral glomerulonephritis (34), it is not an illogical leap that chronic autoimmune inflammation in patients’ kidneys with LN can promote persistent activation of the JAK/STAT pathway in podocytes. The gene discussed is SOAT1; the disease is chronic kidney disease.