Anti-GBM glomerulonephritis has been suggested to be Th1 mediated due to the predominance of the Th1-associated IgG antibody subclasses (IgG1 and/or IgG3) and the presence of delayed-type hypersensitivity (DTH) effectors deposited in the kidney (41). This evidence concerns the gene IGHG3 and glioblastoma.