This environment stimulates the production of proinflammatory cytokines (such as type I IFNs, Tumor Necrosis Factor Alpha (TNF-α), granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-1β, IL-6), and chemokines (such as C-C motif chemokine ligand 2 (CCL2), CCL3, C-X-C motif chemokine ligand 9 (CXCL9), and CXCL10), turning the “cold” tumor into an inflamed, immunologically “hot” tumor [18]. The gene discussed is CCL2; the disease is neoplasm.