Besides type I IFN, tumour lesions also produce high amounts of vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), interleukin-10 (IL-10), transforming growth factor-β (TGF-β), macrophage colony-stimulating factor (M-CSF), cyclooxygenase-2 (COX-2) and gangliosides, which can impair the differentiation, maturation and function of DCs [32] (figure 1b). This evidence concerns the gene TGFB1 and neoplasm.