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Cancer immunity is subjected to spatiotemporal regulation by leukocyte interaction with neoplastic and stromal cells, contributing to immune evasion and immunotherapy resistance. Here, we identify a distinct mesenchymal-like population of endothelial cells (ECs) that form an immunosuppressive vascular niche in glioblastoma (GBM). We reveal a spatially restricted, Twist1/SATB1-mediated sequential transcriptional activation mechanism, through which tumor ECs produce osteopontin to promote immunosuppressive macrophage (Mφ) phenotypes. Genetic or pharmacological ablation of Twist1 reverses Mφ-mediated immunosuppression and enhances T cell infiltration and activation, leading to reduced GBM growth and extended mouse survival, and sensitizing tumor to chimeric antigen receptor T immunotherapy. Thus, these findings uncover a spatially restricted mechanism controlling tumor immunity and suggest that targeting endothelial Twist1 may offer attractive opportunities for optimizing cancer immunotherapy. 

File systems have many configuration parameters. Such flexibility comes at the price of additional complexity which could lead to subtle configuration-related issues. To address the challenge, we study the potential configuration dependencies of a representative file system (i.e., Ext4), and identify a prevalent pattern called multi-level configuration dependencies. We build a static analyzer to extract the dependencies and leverage the information to address different configuration issues. Our preliminary prototype is able to extract 64 multi-level dependencies with a low false positive rate. Additionally, we can identify multiple configuration issues effectively.