Since CXCL10 has been shown to enhance the activity of effector CD4+ and CD8+ T cells and facilitate their migration to sites of inflammation (including tumor microenvironments), inhibiting this chemokine may offer therapeutic benefits for several T cell–driven autoimmune disorders, such as psoriasis, rheumatoid arthritis (RA) [43,44], inflammatory bowel disease [54], and type I diabetes (T1DM) [55], but also ALD as revealed in our study. The gene discussed is CD8A; the disease is inflammatory bowel disease.