Abstract
Several molecular and cellular correlates of melanoma response to checkpoint inhibition have been described, notably tumor programmed death ligand-1 expression, major histocompatibility complex class I expression, mutational load, and T-cell infiltration. The clinical correlation to vitiligo suggests a potential mechanistic link to microphthalmia-associated transcription factor, a transcription factor important in both melanocyte-lineage development and melanocyte survival.