Neonatal T cells have historically been considered relatively unresponsive, leading many to believe that neonates are immunodeficient. Even today, a notion persists that neonatal CD8+ T cells (CTLs), or those critical for protecting the host against intracellular pathogens and cancer, are immature and less reactive than adult counterparts, prompting recommendations for stronger adjuvants or repeated boosting with vaccines. However, we discovered that neonatal CTLs are in fact more reactive than adult T cells. They utilize distinct transcriptional and epigenetic programs, making them intrinsically and uniquely responsive to innate cytokine stimulation. Moreover, we identified key regulators (AP1/BACH2) that can be used to program different-aged CTLs to behave in beneficial ways (e.g., increase their innate-like functions or ability to form long-lived memory cells). Once we dissect out precisely how the AP1/BACH2 axis operates in CTLs, we believe our studies will i) allow us to enhance neonatal memory CTLs to reduce infectious disease burden in children; ii) reveal druggable targets that can be leveraged to design more precise immunotherapies (e.g., CAR-T cells); and iii) pave the way for new therapies that can be used to manipulate the innate functions of CTLs in various settings (e.g., autoimmune diseases and chronic infection).