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The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4+T cells; however, its cell-intrinsic role in CD8+T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8+T cell (TRM) differentiation and function. Genetic ablation of Ahr in mouse CD8+T cells leads to increased CD127–KLRG1+short-lived effector cells and CD44+CD62L+T central memory cells but reduced granzyme-B-producing CD69+CD103+TRMcells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8+T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8+T cells also highly express AHR that regulates in vitroTRMdifferentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8+T cell immunity.