CL-11 in the tumor (locally synthesized and circulation-derived) can contribute to melanoma tumor growth via 2 main pathways: (a) CL-11–induced activation of mitogenic kinase signaling and stimulation of tumor cell proliferation and (b) CL-11–dependent promotion of immunosuppressive TME, characterized by high proportion of myeloid cells and low proportion of lymphocytes, lack of cytotoxic T cell infiltrating in the tumor core, increased angiogenesis, low levels of cytokines/chemokines having antitumor properties, and reprograming macrophages to M2. The gene discussed is COLEC11; the disease is neoplasm.