The idea that LCs may play a role in the down-regulation of the cutaneous immune response is supported by three studies; first, a study in humans showed that immature LCs accumulate in skin-draining lymph nodes in patients with cutaneous infections or malignancies in the absence of autoimmune response such as vitiligo [47]; second, a recent work suggested that mice without LCs have increased skin contact hypersensitivity [48]; a third study showed that environmental stimuli at the skin can redirect the local and systemic immune system by means of RANKL [35]. This evidence concerns the gene TNFSF11 and vitiligo.