One study also showed that interference with both STAT3 and p38 MAPK signaling pathways in monocyte progenitors further improved the quality of tumor-associated DC, blocking the inhibitory effects of tumor-derived factors on DC differentiation from these progenitors and skewing the IL-12/IL-10 cytokine profile of the resulting DC toward a TH1-promoting phenotype (148). The gene discussed is STAT3; the disease is neoplasm.