Recent studies have shown that neonatal CD8+ T cells can undergo ‘bystander activation’ in response to inflammatory cytokines and produce effector molecules such as IFNγ and granzyme B in the absence of cognate antigen. Some of these cells persist into adulthood. A study by Watson et al. used a multi-omics approach to investigate the epigenetic programmes and transcription factors that enable CD8+ T cells to provide innate-like protection. They found that neonatal CD8+ T cells are intrinsically poised to produce cytokines, including some, such as IL-13, IL-10 and GM-CSF, that are not commonly associated with CD8+ T cells. Stimulation of these cells with the inflammatory cytokines IL-12 and IL-18 induces extensive chromatin remodelling and exposes binding sites for AP-1 transcription factors. By contrast, adult CD8+ T cells are less capable of altering chromatin in response to IL-12 or IL-18 stimulation. They also express higher levels of the transcriptional repressor BACH2, which shares binding sites with AP-1 transcription factors and limits the differentiation of effector cells. Overall, their results indicate that neonatal CD8+ T cells are much more functionally diverse than their adult counterparts and represent an intrinsically more innate-like lineage, largely due to their enhanced capacity to undergo chromatin remodelling.