The Vitamin A metabolite retinoic acid (RA) plays a critical role in the regulation of homeostatic and inflammatory T cell responses in the intestine. However, the mechanisms that direct T cell differentiation and function downstream of RA signalling remain unclear. We have recently identified the transcriptional repressor HIC1 (hypermethylated in cancer 1) as an RA-dependent regulator of T cell function in the gut. We have previously shown that HIC1 expression is upregulated by RA, and that mice raised on a Vitamin A-deficient diet lack HIC1-positive immune cells in the intestinal lamina propria and intraepithelial compartment. In vivo deletion of HIC1 in T cells also results in a severe reduction in T cell numbers in the intestine, including the loss of naturally-occurring CD69+ CD103+ tissue resident memory T (TRM) cells. We investigated the link between RA signalling and HIC1 gene repression via in vitro activation of wild-type or HIC1-deficient CD4+ T cells in the presence or absence of RA, and analysed changes in global gene expression by RNA-seq. In the absence of HIC1 and independently of RA, we found a significant upregulation of genes associated with Myc-dependent regulation of metabolic processes such as glycolysis and lipid oxidation. Further, of a suite of 57 genes known to be significantly downregulated in TRM cells, 52 genes (91%) were downregulated by RA treatment in our study. In the absence of HIC1, RA-mediated downregulation was reduced or abolished in 47 of these genes (82%), suggesting that RA signalling through HIC1 may play a central role in driving gene expression profiles in tissue residency, possibly by regulating T cell metabolic pathways. Further investigation of RA and HIC1 function during immunity and inflammation may provide novel therapeutic targets in the treatment of T cell-driven inflammatory diseases in the intestine.