Additionally, the pro-inflammation factor interferon (IFN-γ) released by CD8+ T cells can induce the production of chemokines including C-X-C motif chemokine ligands 9 and 10 (CXCL9 and CXCL10) via JAK-STAT signaling in keratinocytes, fibroblasts or other skin cells [8, 9], which in turn can interact with their receptor C-X-C Motif Chemokine Receptor 3 (CXCR3) and promote CXCR3+CD8+ T cells recruiting to the melanocytes, exacerbating the progression of vitiligo [10, 11]. The gene discussed is IFNG; the disease is vitiligo.