Although immune checkpoint blockade (ICB) has shown success in prolonging the survival of patients with cancer, the mechanisms behind this are not fully elucidated. Chen et al. find that tumor-derived IL33, whose expression increases after ICB treatment, and ST2 signaling in nontumor cells are key to inducing antitumor responses. IL33 increases functional CD103⁺CD8⁺ T cells and CD103⁺ dendritic cells (DC) in the tumor microenvironment (TME), and the CD103⁺ DCs are essential for the recruitment of tumor-infiltrating CD8⁺ T cells into the TME. By treating tumor-bearing mice with IL33 in combination with dual ICB, survival was extended, highlighting the important role of IL33 in mediating the efficacy of ICB. Read more in this issue on page 1381. Original image from Fig. 4F. Artwork by Lewis Long.