This finding suggests that cytokine-activated TRM cells cause the pathogenesis of vitiligo; as in patients with alopecia areata, overproduction of IL-2 or IL-15 by non-TRM cells somehow activates NKG2D expression on CD103+CD8+ TRM-like cells to secrete Prf1 and GzmB in a TCR-independent manner [228]. The gene discussed is PRF1; the disease is vitiligo.