Apolipoproteins, which can play a potential role in FSGS pathogenesis as “permeability factors” [116], as well as proteins whose roles are not yet completely understood, such as lysosome membrane protein-2 and afamin in MN [56,57] and the laminin G-like 3 (LG3) fragment of endorepellin in IgAN [64], may reflect pathological processes and could become targets for new approaches to immunosuppressive or nephroprotective therapy. This evidence concerns the gene HSPG2 and focal segmental glomerulosclerosis.