Importantly, combined interference in the STAT3 and p38 pathways completely prevented inhibition of DC differentiation by all tested tumor supernatants (n = 18, derived from both primary tumors and tumor cell lines, together encompassing eight different histological origins) and led to superior DC functionality, evidenced by increased allogeneic T cell reactivity with elevated IL-12p70/IL-10 ratios and Th1 skewing (32). Here, STAT3 is linked to neoplasm.