A cardinal 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. Eomesodermin (Eomes) is a transcription factor that has previously been reported to play a role in the development of the memory CD8 T cell pool (1). However, the molecular mechanism governing its role in memory CD8 T cell programming and/or maintenance remain unclear. Herein we sought to determine whether Eomes played a role in either the programming or maintenance of the memory CD8 T cell pool, or influenced both of these factors. By combining adoptive transfer of both WT and Eomes deficient (Eomes-/-) TCR transgenic CD8 T cells with localized, recombinant influenza infection, we demonstrate that Eomes-/- T cells are unable to generate and maintain effective memory CD8 T cells compared to WT controls. This defect was particularly apparent in central memory cells but less so in effector memory populations. Interestingly, the lower number and frequency of CD8 memory T cells in the absence of Eomes does not affect their ability to respond to a secondary challenge both quantitatively and functionally. Taken together, this data suggests that Eomes is important for the maintenance of the memory CD8 T cells and does not appear to be essential for their programming as defined by their ability to mount a response to a subsequent challenge. Moreover, this subtle phenotype is supported by RNAseq data demonstrating that globally the transcriptome is very similar between memory CD8 T cells lacking Eomes and WT controls. Current work investigating the role of genes that differed in our RNAseq analysis and the molecular targets of Eomes will allow us to determine the molecular mechanism by which Eomes is influencing memory CD8 T cell maintenance.