CXCR3 binds to CXCL9 and CXCL10, recruiting additional MC-reactive T cells and perpetuating existing vitiligo lesions through a self-reinforcing “IFN-γ–CXCL axis.” (9, 10) Single-cell RNA sequencing reveals that lesional TRM cells exhibit a twofold increase in IFN-γ production compared to healthy skin, highlighting their role as a primary source of cytokines and their functional significance. The gene discussed is IFNG; the disease is vitiligo.