Epidermal melanocyte loss in vitiligo, triggered by stresses ranging from trauma to emo-tional stress, chemical exposure or metabolite imbalance, to the unknown, can stimulate oxidative stress in pigment cells which secrete damage-associated molecular patterns that then initiate innate immune responses. Antigen presentation to melanocytes leads to stim-ulation of autoreactive T cell responses, with further targeting of pigment cell. Studies show a pathogenic basis for cellular stress, innate immune responses and adaptive immun-ity in vitiligo. Improved understanding of the aetiological mechanisms in vitiligo has already resulted in successful use of the Jak-1 inhibitors in vitiligo. In this review we outline the cur-rent understanding of the pathological mechanisms in vitiligo, and locate loci to which therapeutic attack might be directed.