The affinity of the T-cell receptor (TCR) for antigen is central to determining T-cell fate both during development in the thymus and during peripheral activation and differentiation. While some differential signaling has been described between low- and high-affinity TCR-antigen interactions, the mechanisms through which antigen affinity determine T-cell fate are still poorly defined. In a recent issue of Nature Immunology, Man et al.1 make the novel insight that the transcription factor IRF4 links antigen-TCR affinity to important metabolic changes that are required to generate an effective CD8+ T-cell effector response.1