The latest Japanese study of Yuka Nishibata et al has suggested that the release of ANCA can damage the kidney and then result in revealing α3(IV)NC1, leading to infiltration of CD11c+ macrophages, subsequently the exposed GBM epitope can induce the formation of anti-GBM antibodies (22, 23), which can explain why DPPs have similar characteristics to anti-GBM disease. This evidence concerns the gene ITGAX and glioblastoma.