T-cell fate is shaped by the strength and duration of activation signals, which impacts the epigenetic programs that influence differentiation. In this work, we systematically profiled epigenetic modulators to define how they influence T-cell differentiation. We establish that inhibitors targeting lysine acetylation dynamics play a key role in controlling T cell fate; a dual CBP/p300 catalytic inhibitor induces a central memory phenotype when added to T-cells prior to the first cell division, while a histone deacetylase inhibitor promotes effector differentiation. CBP/p300 are paralogous histone acetyltransferases that exhibit functional redundancy, compensating for one another when one is missing. Yet, Crebbp is the second most frequently mutated chromatin modifying gene in follicular and B-cell lymphoma, and its inactivation in mouse models has oncogenic consequences. This underscores that despite the overlapping roles of CBP and p300, each governs distinct regulatory programs. The roles of CBP and p300 in T-cells remain undefined as they have long been considered functionally equivalent. To bypass this we developed an inducible degron mouse model enabling temporal control of CBP or p300 protein levels in T-cells, independently. The transient loss of CBP alone prior to the first division is sufficient to drive a memory signature, closely mirroring the effects observed with the dual catalytic inhibitor. This is further reflected at the epigenetic level by a pronounced reduction in histone acetylation, most notably in H2BK20ac. Comparatively, profiling in p300 degron T-cells further highlights distinct, non-redundant motifs that are impacted by CBP loss. These findings uncover a temporal requirement for CBP in establishing effector T-cell identity where its loss redirects differentiation towards a memory fate, and it provides mechanistic insight into how selective epigenetic perturbation can be leveraged to improve CAR T-cell therapy.