hBD-3 induces monocyte activation through both P2X7-dependent (CD86 upregulation) and P2X7-independent (CD80 upregulation) signaling mechanisms, which raises the possibility that activation of P2X7R might play an important role in shaping the inflammatory microenvironment under conditions in which hBD-3 is highly expressed, such as in psoriasis or oral carcinoma [127]. Here, P2RX7 is linked to lip and oral cavity carcinoma.