By stimulating CXCL9 production driven by cDC1, anti-TIM-3 therapy activates robust CD8+ T cell responses within the tumor, heightening sensitivity to paclitaxel chemotherapy.426 Therefore, the limited efficacy in highly inflamed tumor patients could be attributed to the reduced presence of TCF-1+ cells and/or impediments hampering their interaction with cDC1 in the tumor microenvironment. This evidence concerns the gene HAVCR2 and neoplasm.