A recent report has described a higher expression level of SF2/ASF in many tumors, including lung, thyroid, kidney, colon, small intestine and melanoma, relative to their respective normal controls. One mechanism to explain this observation is that SF2/ASF abolished the tumor suppressor activity of BIN1, a tumor suppressor gene, by inclusion of exon 12A which interferes with MYC binding (45) . In contrast to its roles in transplantation, autoimmune diseases and inflammation, CD200 enhances the growth of malignant tumors and it has been suggested that a novel approach to anticancer therapy might include blockade of CD200 (15, 16, (46) (47) (48) (49) . Since CD200 tr is an antagonist to CD200 (27) , our data are consistent with the hypothesis that increased CD200 tr expression and decreased expression of full-length CD200 by blockade of SF2/ASF may also be of potential benefit for cancer treatment.