A recent study revealed that treatment with VEGF blockade agents in a glioma mouse model leads to increased expression of SLC7A11, and it was proposed that glutamate exported by SLC7A11 from tumor cells then promotes the proliferation and immunosuppressive function of regulatory T-cells (Tregs), which contributes to adaptive resistance to anti-VEGF therapy in glioblastoma (Long et al., 2020). The gene discussed is VEGFA; the disease is glioblastoma.