CD248 and neoplasm: Although lack of TEM1/endosialin expression did not inhibit brain tumor growth in our model, the cell surface bioavailability of TEM1/endosialin and its localization to tumor and tumor vasculature components in both primary and metastatic brain tumors, both diseases with limited current treatment options, support efforts to target this protein with alternative approaches, including antibody or antibody-cytotoxin based strategies, such as a recently reported anti-TEM1/endosialin IgG conjugated to saporin, and other efforts in pre-clinical development [11,21,33] or as combination therapy.