Researchers utilizing a CXCL9-deficient mouse model of vitiligo observed a decreased number of premelanosome protein-specific (PMEL) CD8+ T cells in both the dermis and epidermis; however, the deficiency in CXCL9 did not reverse the disease or reduce depigmentation significantly in mice with established vitiligo, which further confirmed the role of CXCL9 as a “recruit” signal in positioning and recruiting T cells [56]. The gene discussed is CD8A; the disease is vitiligo.