Using our previously established ssRNA-sh-Pim-3 dual-function vector, which both silences the proto-oncogene Pim-3 to promote apoptosis of tumor cells and simultaneously activates TLR7 to stimulate antitumor immune responses (8, 25), we verified that the dual-function vector not only promotes apoptosis and inhibits proliferation of B16F10 melanoma cells but also stimulates the activation of pDCs to secrete a large amount of type I IFN. The gene discussed is PIM3; the disease is neoplasm.