Adoptive T cell therapy (ACT) is a promising immunotherapeutic approach to fight cancer by utilizing cytotoxic T lymphocytes (CTL), which specifically target and eradicate tumour cells. However, one major limitation of this therapy is the ability of tumours to interfere with the CTL through immune escape mechanisms. In a mouse model of B-cell lymphoma and ACT, we investigated the mechanisms underlying this failure. We found that tumour-specific CTL fail to eradicate lymphoma cells once the tumour burden reaches a certain threshold. In this case a major proportion of the CTL is rapidly deleted and those remaining lose their effector function, a process we call “stunning”. We hypothesis that nutrient deprivation could be one tumour immune escape mechanism to inhibit T cell function. By consuming high amounts of glucose, tumours limit the glucose access to tumour infiltrating T lymphocytes, which can impair their glycolysis and effector functions. To investigate whether stunning is induced by the lymphoma cells out competing the CTL for nutrients such as glucose, we analyze tumour as well as T cell metabolism by mutating the expression of metabolism associated genes in these cells.