Interferon (IFN)-γ signaling promotes the progression of CD8+ T cell-mediated autoimmune skin diseases, such as lupus erythematosus, alopecia areata, vitiligo, and lichen planus.1, 2, 3, 4 Autoreactive CD8+ T cells in lesional skin produce IFN-γ that binds the IFN-γ receptor to activate the Janus kinase (JAK)-signal transducer and activator of transcription pathway, thereby stimulating the expression of IFN-γ-inducible chemokines, such as CXCL9, CXCL10, and CXCL11. The gene discussed is CD8A; the disease is vitiligo.