Tissue resident memory T (TRM) cells have emerged as a distinct subset of the memory T cell pool, characterised by preferential localisation within the tissue of primary infection. Broadly, CD8+ TRM cells can be identified by expression of cell surface proteins CD69 and CD103, but alone are imperfect markers. Another shared feature among TRM populations is the downregulation of a repertoire of pro-migratory genes, aiding retention. A methodology to model TRM cells robustly in vitro is yet to be described, prompting a key aim of this project. Doing so, would accelerate our ability to fully understand the molecular mechanisms regulating these sentinels of tissue immunity, opening the door to potential therapeutic modulation in disease settings. In this study, CD8+ T cells were enriched from murine splenocytes and cultured for 7 days. Strikingly, flow cytometry analysis showed that samples treated with retinoic acid (RA) as well as TGFβ, a known mediator of TRM cell development, dramatically increased CD69+CD103+ proportions, in comparison to conditions lacking these constituents. Bulk RNA sequencing analysis demonstrated that transcriptional repression seen in bona fide TRM cells, was also largely reflected by our in vitro TRM model. Hypermethylated in Cancer 1 (HIC1) is an RA-dependant transcriptional repressor. Cells cultured from T cell intrinsic Hic1-deficient mice experienced a ~75% reduction in CD69+CD103+ frequency. Furthermore, transcriptional analysis by qPCR revealed an essential role for HIC1 in regulating the repression of pro-migratory genes in our in vitro TRM model. Taken together, in generating a novel cell culture methodology to generate TRM-like populations, our results indicate instrumental roles for atRA and HIC1 in the development of CD8+CD69+CD103+ cells in vitro.