Many studies have shown that all three pathways of complement activation may be involved in kidney injury in diabetic nephropathy through C1q, C3, and C5 components (i.e., the classic pathway), mannose binding lectin (MBL) activator (i.e., the lectin pathway), and TLR2 and TLR4 (i.e., the alternative pathway), which can increase complement factor B synthesis and release by macrophages. The gene discussed is TLR2; the disease is diabetic kidney disease.