Mechanistically, cancer-associated fibroblasts promote immune tolerance by secreting CXCL12 and CCL17, thereby recruiting regulatory T cells and reinforcing a suppressive stromal niche; melanoma-derived factors and metabolic perturbations reprogram tumor-associated macrophages toward a pro-tumoral phenotype through lipid metabolic remodeling, endoplasmic reticulum stress, and immunosuppressive mediator production; and hypoxic stress amplifies CD39/CD73-dependent adenosine generation, which suppresses dendritic cell maturation and cytotoxic T-cell activity while facilitating immune escape. The gene discussed is CCL17; the disease is melanoma.