In this setting, BRAF mutations play a complex role by: i) directly increasing cancer cell proliferation, ii) influencing the immune cell composition of tumor microenvironment, thus creating local immune-suppression, which favors the tumor immune-escape, iii) inducing a greater secretion of pro-tumorigenic chemokines (CXCL8, CCL2), which in turn promotes cancer cell proliferation, angiogenesis and metastatization. This evidence concerns the gene CCL2 and neoplasm.