MN can be classified as either primary or secondary, based on the identifiable causes.[1] Primary MN is caused by antibodies directed against target antigens located on the glomerular podocyte; the primary target antigens are M-type phospholipase A2 receptor (PLA2R)[2] and thrombospondin type-1 domain-containing 7A (THSD7A).[3] Secondary MN can arise from conditions that include autoimmune diseases, malignancies, and infections. This evidence concerns the gene THSD7A and autoimmune disease.