IL-17 promotes tumor growth through the IL-6-Stat3 signaling pathway. This study shows that IL-17 enhances tumor growth in B16 melanoma and MB49 bladder carcinoma, while its absence reduces tumor growth. IL-17 is primarily produced by CD4+ T cells and acts directly on tumor cells and stromal cells, which express IL-17 receptors. IL-17 induces IL-6 production, which activates Stat3, up-regulating genes involved in tumor survival and angiogenesis. The Th17 response promotes tumor growth, in part via the IL-6-Stat3 pathway. IL-17 and IFN-γ have a reciprocal relationship in tumors, with IL-17 enhancing IFN-γ production in the absence of IFN-γ. IL-17 activates Stat3 in both tumor and stromal cells, leading to the up-regulation of oncogenic genes. IL-6 is a key mediator in this process, as IL-17 stimulates IL-6 production, which in turn activates Stat3. In vivo, blocking IL-6 reduces tumor growth and Stat3 activity. These findings suggest that IL-17 promotes tumor growth through IL-6-Stat3 signaling, highlighting the role of Th17 cells in cancer progression. The study also underscores the complex interplay between immune cells and tumor microenvironment in cancer development.IL-17 promotes tumor growth through the IL-6-Stat3 signaling pathway. This study shows that IL-17 enhances tumor growth in B16 melanoma and MB49 bladder carcinoma, while its absence reduces tumor growth. IL-17 is primarily produced by CD4+ T cells and acts directly on tumor cells and stromal cells, which express IL-17 receptors. IL-17 induces IL-6 production, which activates Stat3, up-regulating genes involved in tumor survival and angiogenesis. The Th17 response promotes tumor growth, in part via the IL-6-Stat3 pathway. IL-17 and IFN-γ have a reciprocal relationship in tumors, with IL-17 enhancing IFN-γ production in the absence of IFN-γ. IL-17 activates Stat3 in both tumor and stromal cells, leading to the up-regulation of oncogenic genes. IL-6 is a key mediator in this process, as IL-17 stimulates IL-6 production, which in turn activates Stat3. In vivo, blocking IL-6 reduces tumor growth and Stat3 activity. These findings suggest that IL-17 promotes tumor growth through IL-6-Stat3 signaling, highlighting the role of Th17 cells in cancer progression. The study also underscores the complex interplay between immune cells and tumor microenvironment in cancer development.