Moreover, IL‐1 can bind to IL‐1R1 on fibroblasts, activating fibroblasts and promoting their differentiation into inflammatory cancer‐associated fibroblasts (iCAFs) that release various inflammatory factors, further shaping an immunosuppressive TME.[21, 32] Through the in vivo mouse experiments, we demonstrated that combined targeting IL‐1/IL‐1R1 could improve the TME of IS subtype tumor (YTN5), thereby significantly enhances its sensitivity to immunotherapy. Here, IL1A is linked to neoplasm.