While IPH2102 blocked KIR-inhibitory signaling on the NK cells, Lenalidomide activated them to increase production of TNF-α, IFN-γ, and granzyme B. The tumor can also be sensitized to autologous NK cells by coadministering proteosome inhibitors (e.g., Bortezomib), doxorubicin, or histone deacetylase inhibitors that upregulate stress ligands for NKG2D receptors, induce pro-inflammatory cytokines or death receptors that bind TNF-α. The gene discussed is IFNG; the disease is neoplasm.