It has been shown that upon recognition of bacteria-infected or tumor cells, activated Vγ9Vδ2+ T cells can aid DC maturation through cytokine secretion (IFN-γ and TNF-α) (87, 88), and promote maturation of antigen-expressing immature DCs (monocyte-derived) in circulation via contact-dependent mechanisms (Fas/FasL, CD40/CD40L, and TCR/CD1) independent from TLR signaling (89–91, 93) (Figure 2). This evidence concerns the gene CD1C and neoplasm.