The molecular pathways underlining the protective effect of KLK in anti-GBM-GN is not yet fully understood, but the close correlation between the levels of KLK and GSTM2 in the renal tissue of anti-GBM-GN mice implies that GSTM2 might be one of the effector molecules involved in ameliorating inflammation and oxidative stress during the course of autoantibody-induced nephritis [17,18,36,37]. The gene discussed is GSTM2; the disease is ganglioneuroma.