In such contexts, CXCL10 signaling may indirectly facilitate immune escape, particularly when enhanced by STAT3 activation or a hypoxic tumor microenvironment.50,51 Although CXCL10 is generally associated with the promotion of antitumor immunity, there is evidence that in certain tumor situations it can paradoxically promote metastasis through interactions with stromal components of the tumor microenvironment, such as fibroblasts, endothelial cells, and stromal macrophages. The gene discussed is STAT3; the disease is neoplasm.