Interleukin‐7 (IL‐7) is a crucial cytokine involved in T‐cell survival and development but its signalling in human T cells, particularly in effector/memory T cells, is poorly documented. In this study, we found that IL‐7 protects human CD4⁺ effector/memory T cells from apoptosis induced upon the absence of stimulation and cytokines. We show that IL‐7 up‐regulates not only Bcl‐2 but also Bcl‐xL and Mcl‐1 as well. Interleukin‐7‐induced activation of the janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling pathway is sufficient for cell survival and up‐regulation of Bcl‐2 proteins. In contrast to previous studies with naive T cells, we found that IL‐7 is a weak activator of the phosphatidylinositol 3 kinase (PI3K)/AKT (also referred as protein kinase B) pathway and IL‐7‐mediated cell survival occurs independently from the PI3K/AKT pathway as well as from activation of the mitogen‐activated protein kinase/extracellular signal‐regulated kinase pathway. Considering the contribution of both IL‐7 and CD4⁺ effector/memory T cells to the pathogenesis of autoimmune diseases such as rheumatoid arthritis and colitis, our study suggests that IL‐7 can contribute to these diseases by promoting cell survival. A further understanding of the mechanisms of IL‐7 signalling in effector/memory T cells associated with autoimmune inflammatory diseases may lead to potential new therapeutic avenues.