In vitro experimental models of glioma cell-intrinsic mechanisms revealed that IDH mutation may inhibit recruitment of CD8 + T cells via CXCL10 downregulation [16], while Sarah and his team observed that treatment with GSK343 modulated the innate immune response in GBM by elevating CXCL9, CXCL10, and CXCL11 expression levels, enhancing the migration of NK cells to tumor sites and consequently promoting NK cell-mediated tumor growth inhibition [17]. Here, CXCL11 is linked to neoplasm.