Core Viewpoint - Vitiligo is an autoimmune disease affecting approximately 0.5%-2% of the global population, characterized by white patches on the skin due to the attack of autoreactive CD8+ T cells on melanocytes. Recent research has identified a novel mechanism involving sensory neurons and CGRP that enhances CD8+ T cell responses, suggesting new therapeutic strategies for treatment [1][6][11]. Group 1: Disease Mechanism - The study reveals a new pathogenic mechanism in vitiligo involving a "sensory neuron-CGRP-cDC1-CD8 T cell" axis, where CGRP enhances the function of dermal type I conventional dendritic cells (cDC1) to drive autoreactive CD8 T cell responses [3][7][12]. - CD8+ T cells kill melanocytes in vitiligo, but the specific immune pathogenesis and ideal drug targets remain unclear [6]. Group 2: Therapeutic Development - Ruxolitinib cream, a selective JAK1/2 inhibitor, is the first approved treatment for non-segmental vitiligo, but it has a clinical response rate of about 30% and is associated with adverse events [1]. - The CGRP receptor antagonist Rimegepant has shown significant disease progression inhibition in mouse models and promising results in a clinical trial involving 57 vitiligo patients, indicating a new treatment strategy [3][8][11]. Group 3: Clinical Trial Insights - A clinical trial divided 57 vitiligo patients into three groups to assess the efficacy of Rimegepant cream combined with phototherapy, showing that the cream significantly improved skin repigmentation rates [8][11]. - The study utilized single-cell sequencing and spatial transcriptomics to analyze skin lesions, providing insights into the immune interactions involved in vitiligo [3][7].