Alopecia areata (AA) and vitiligo are distinct autoimmune diseases characterized by non-scarring hair loss and skin pigment loss, respectively. Both diseases share common pathogenic mechanisms, including immune privilege collapse, activated IFN-γ signaling, and involvement of cytotoxic CD8+ T lymphocytes. However, they differ in the location of inflammatory infiltrates and the specific immune pathways involved. AA involves inflammatory cells in the deep reticular dermis near the hair bulb, while vitiligo involves infiltrates in the epidermis and papillary dermis. Both diseases are associated with oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway. Common factors include immune privilege collapse, enhanced expression of MHC molecules, and the role of plasmacytoid dendritic cells in producing IFN-α. Blood chemokines CXCL9 and CXCL10 are elevated in both diseases. AA and vitiligo also share susceptibility genes, such as CTLA4, HLA, and IL2Rα. Despite these similarities, differences in pathogenesis include the location of immune privilege collapse and the specific DAMPs involved. AA is associated with MICA and ULBP3, while vitiligo involves HSP70. Both diseases are linked to immune privilege collapse, but vitiligo has less explored evidence of this process. The review highlights the shared and distinct pathogenic mechanisms between AA and vitiligo, emphasizing the importance of understanding these differences for developing targeted therapies.Alopecia areata (AA) and vitiligo are distinct autoimmune diseases characterized by non-scarring hair loss and skin pigment loss, respectively. Both diseases share common pathogenic mechanisms, including immune privilege collapse, activated IFN-γ signaling, and involvement of cytotoxic CD8+ T lymphocytes. However, they differ in the location of inflammatory infiltrates and the specific immune pathways involved. AA involves inflammatory cells in the deep reticular dermis near the hair bulb, while vitiligo involves infiltrates in the epidermis and papillary dermis. Both diseases are associated with oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway. Common factors include immune privilege collapse, enhanced expression of MHC molecules, and the role of plasmacytoid dendritic cells in producing IFN-α. Blood chemokines CXCL9 and CXCL10 are elevated in both diseases. AA and vitiligo also share susceptibility genes, such as CTLA4, HLA, and IL2Rα. Despite these similarities, differences in pathogenesis include the location of immune privilege collapse and the specific DAMPs involved. AA is associated with MICA and ULBP3, while vitiligo involves HSP70. Both diseases are linked to immune privilege collapse, but vitiligo has less explored evidence of this process. The review highlights the shared and distinct pathogenic mechanisms between AA and vitiligo, emphasizing the importance of understanding these differences for developing targeted therapies.