PMN is considered a renal‐limited, autoantibody‐induced, complement‐mediated, podocyte‐targeted autoimmune disease.[3, 4, 5, 16] The histopathological characteristic of PMN is GBM thickening and the formation of subepithelial “spikes” due to ECM accumulation.[4] COL4A3 and COL4A4 are two of the major ECM components of GBM,[11] observed to be upregulated in both human and experimental MN,[34] but their upstream regulator remains largely unclear. The gene discussed is COL4A4; the disease is autoimmune disease.