Since our studies have indicated that tumor-derived TGF-β is capable of inducing IDO expression by pDCs and that this effect is enhanced upon loss of TβRIII in a murine breast cancer model, we investigated the ability of an oral type I TGF-β receptor serine/threonine kinase inhibitor (SM16) to augment the immunologic response of a Her2/neu vaccine. The gene discussed is MARK2; the disease is breast carcinoma.