The success of cancer immunotherapy is limited by potent endogenous immune‐evasion mechanisms, which are at least in part mediated by transforming growth factor‐β (TGF‐β). The E3 ubiquitin ligase Cbl‐b is a key regulator of T cell activation and is established to regulate TGF‐β sensitivity. cblb‐deficient animals reject tumors via CD8+ T cells, which make Cbl‐b an ideal target for improvement of adoptive T‐cell transfer (ATC) therapy. In this study, we show that cblb‐deficient CD8+ T cells are hyper‐responsive to T‐cell receptor (TCR)/CD28‐stimulation and are in part protected against the negative cues induced by TGF‐β in vitro. Notably, adoptive transfer of polyclonal, non‐TCR transgenic cblb‐deficient CD8+ T cells is not sufficient to reject B16‐ova or EG7 tumors in vivo. Thus, cblb‐deficient ATC requires proper in vivo re‐activation by a dendritic cell (DC) vaccine. In strict contrast to ATC monotherapy, this approach delayed tumor outgrowth and significantly increased survival rates, which is paralleled by increased CD8+ T‐cells infiltration to the tumor site and enrichment of ova‐specific and interferon‐γ (IFN‐γ)‐secreting CD8+ T cell in the draining lymph node (LN). Moreover, CD8+ T cells from cblb‐deficient mice vaccinated with the DC vaccine show increased cytolytic activity in vivo. In summary, our data using cblb‐deficient polyclonal, non‐TCR‐transgenic adoptively transferred CD8+ T cells into immuno‐competent non‐lymphodepleted recipients suggest that targeting Cbl‐b might serve as a novel ‘adjuvant approach’, suitable to augment the effectiveness of established anti‐cancer immunotherapies.