showed that CD28-B7 checkpoint blockade with an agonistic monoclonal antibody, CTLA4-Ig, that selectively binds to B7.1, reduced autoantibody production and cellular infiltration of glomeruli in an experimental autoimmune rat model of Goodpasture’s disease.[18] Kitching and colleagues further corroborated these findings with an elegant murine study, showing that in humorally mediated anti-GBM GN induced by a foreign antigen, limiting antibody-mediated injury using CTLA4-Fc treatment can attenuate anti-GBM GN.[19]. This evidence concerns the gene CD80 and glioblastoma.