After treatment with anti-PD-1 and anti-CTL antigen-4 (CTLA-4) monoclonal antibodies (mAbs), IL-33 induced in tumor cells led to the improved anti-tumor efficacy of checkpoint inhibitors by increasing the accumulation and effector function of tumor-resident CD103+CD8+ T cells and the numbers of CD103+ DC in the TME. The gene discussed is IL33; the disease is neoplasm.