Alopecia areata (AA) and vitiligo are distinct autoimmune diseases characterized by nonscarring hair loss and skin pigment loss, respectively. Both diseases share commonalities in their pathogenesis, including the involvement of plasmacytoid dendritic cells, interferon-α (IFN-α) signaling pathways, and cytotoxic CD8+ T lymphocytes. Immune privilege collapse, characterized by the downregulation of immunomodulatory factors and enhanced expression of major histocompatibility complex (MHC), is a key feature in AA pathogenesis. In contrast, the immune privilege collapse in vitiligo is less explored. Common factors contributing to both diseases include oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway. CXCL9 and CXCL10 are elevated in both AA and vitiligo, and autoantibodies against tyrosine hydroxylase are present in both conditions. The involvement of type 2 cytokines and Wnt/β-cylcatenin signaling pathways is also discussed. The differences between AA and vitiligo include the location of inflammatory cell infiltration, identified danger-associated molecular patterns (DAMPs), and the robust evidence of immune privilege collapse in AA.Alopecia areata (AA) and vitiligo are distinct autoimmune diseases characterized by nonscarring hair loss and skin pigment loss, respectively. Both diseases share commonalities in their pathogenesis, including the involvement of plasmacytoid dendritic cells, interferon-α (IFN-α) signaling pathways, and cytotoxic CD8+ T lymphocytes. Immune privilege collapse, characterized by the downregulation of immunomodulatory factors and enhanced expression of major histocompatibility complex (MHC), is a key feature in AA pathogenesis. In contrast, the immune privilege collapse in vitiligo is less explored. Common factors contributing to both diseases include oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway. CXCL9 and CXCL10 are elevated in both AA and vitiligo, and autoantibodies against tyrosine hydroxylase are present in both conditions. The involvement of type 2 cytokines and Wnt/β-cylcatenin signaling pathways is also discussed. The differences between AA and vitiligo include the location of inflammatory cell infiltration, identified danger-associated molecular patterns (DAMPs), and the robust evidence of immune privilege collapse in AA.