Gruber et al. (158) suggested that Cbl-b deficiency promotes spontaneous rejection of TC-1 tumors, whereas Cbl-b−/− mice crossed with CD4Cre- SMAD7fl/fl mice abrogates anti-tumor immunity, thus highlighting the importance of Cbl-b deficient T cells in anti-tumor immunity and the ability of these T cells to potentially overcome TGF-β receptor signaling. The gene discussed is CBLB; the disease is neoplasm.