showed that in tumor cells, IDO1 suppressed the antitumor immune response by increasing the expression of complement factor H (CFH) and factor H-like protein 1 (FHL-1) instead of its association with Trp metabolism in human glioblastoma, and there was a survival advantage mediated by ICIs requiring non-tumor cell IDO1 enzyme activity in mouse glioblastoma. This evidence concerns the gene CFH and neoplasm.