Several studies have demonstrated that TIM-3 expression in tumors may contribute to cancer cell immune escape via different mechanisms, including (1) inhibiting CD4+ T cell activation via the IL-6-STAT3 pathway, thereby preventing Th1 polarization and promoting tumor occurrence, growth, and metastasis [42, 63], (2) reducing the adhesion of tumor cells and promoting the survival of melanoma cells [39, 60]. The gene discussed is STAT3; the disease is neoplasm.