In this context, the possibilities are i) the IFN-γ consumption by immune cells against B-ALL, since at D28 the tumor cells were cleared from BM by chemotherapy (as shown in Table 1, mean tumor cells counting in bone marrow aspirate under 7%) and ii) that IRF3 super expression at D28 was enough to induce the production of IFN-γ by cells from BM niche, more than those in the PB (as demonstrated in the box of Figure 7). The gene discussed is IFNG; the disease is neoplasm.