From a pharmacodynamic perspective, ribociclib-induced vitiligo may occur through multiple pathways: the agent significantly inhibits the immunoregulatory function of regulatory T cells (Treg), leading to loss of normal immune surveillance and subsequent autoreactive CD8+ T cell-mediated targeting of melanocytes; in vitro experiments confirm that CDK4/6 inhibitors can directly arrest melanocyte cycle progression and induce programmed cell death (19). The gene discussed is CD8A; the disease is vitiligo.