The authors related these effects to miR-125 targeting of interferon regulatory factor 4 (IRF4) and also observed that, upon forced expression of miR-125b, macrophages adopted an M1 cytotoxic phenotype, presented elevated responsiveness to IFN-γ, and were more effective in killing EL4 T-lymphoma tumor cells in vitro and in vivo [43]. The gene discussed is IRF4; the disease is neoplasm.