In conclusion, we have clearly shown a cross talk between macrophages and L929 tumorcells, in the absence of any exogenous cytokines, which stimulates murine residentmacrophages to produce NO and became cytotoxic by an IRF-1 dependent andcontact-independent route (Fig. 8).In addition we showed that type I and type II IFNs are partially involved in themacrophage stimulation by L929 tumor cell. This evidence concerns the gene IRF1 and neoplasm.