Since CLEC2B can be up-regulated by toll-like receptor stimulation [76], and topical imiquimod (an activator of the toll-like receptors) has been shown to induce vitiligo [78], [79], [80], we speculate that the increased expression of CLEC2B is a reflection of the activated innate immune system in vitiligo skin. The gene discussed is CLEC2B; the disease is vitiligo.