The study [10] found that, compared with the healthy group, the expression of miRNA-186 in the kidney tissue of patients with membranous nephropathy was significantly downregulated, and in vitro experiments proved that miRNA-186 via Toll-like receptor 4 (TLR4), P2X7, and caspase-3 participates in podocyte apoptosis, leading to increased basement membrane permeability, which in turn leads to membranous nephropathy. This evidence concerns the gene CASP3 and membranous glomerulonephritis.