CD4 and CD8 Trm were increased in the lamina propria of inflamed IBD tissue in this study, and T cell transfer colitis experiments in mice confirmed that T cells adopt a Trm phenotype soon after recruitment to lamina propria in active disease.37 The pathological role of Trm was dependent on their pro-inflammatory cytokine production regulated by Hobit/Blimp-1 transcription factors expressed in Trm. The gene discussed is CD8A; the disease is inflammatory bowel disease.