A specialized feature of adaptive CD8+ T cell immunity is the establishment of memory T cells that are capable of rapid and robust responses upon re-infection. Whilst memory T cells provide the basis of CTL-mediated immunity to a secondary infection, the molecular factors that regulate memory T cell formation are far from clear. Eomesodermin (Eomes) is a transcription factor involved in CD8+ T cell differentiation, particularly the formation of memory CD8+ T cells following infection. Here, we sought to determine what role Eomes plays in a localized influenza infection. Using an adoptive transfer model, we demonstrate that there was a significant reduction in the number of Eomes knock-out (EKO) memory T cells, compared to wildtype controls. In addition to being numerically deficient, EKO memory T cells expressed lower levels of IL-2Rβ, suggesting this difference could be due to a defect in homeostatic proliferation. Interestingly EKO cells in the lung, the site of infection, show a significant increase in the expression of CD103, a marker of tissue resident memory cells. Furthermore, the fold change in WT/EKO cells followed a site specific hierarchy of bone marrow > spleen > lung. This data combined suggests that following viral clearance, Eomes is essential for cell egress from the site of infection and the generation of a stable memory pool in primary and secondary lymphoid organs. Further work aims to determine whether this preference is due to the inability of EKO cells to receive the appropriate signals in order to differentiate into central memory cells due to their location, or if it is a defect in the programming of the cells.