Given the dual-targeting of JOC-x to DSG2 and poly(I:C) to TLR3, we predict our JOC-poly(I:C) may exhibit dose sparing qualities by resulting in less non-specific binding of poly(I:C) to non-tumor TLR3 cells as well as targeting the host-directed therapeutic to tumors. The gene discussed is TLR3; the disease is neoplasm.