TSHR and geroderma osteodysplastica: TSHR is considered the primary autoantigen in GO, and orbital fibroblasts (OFs) are the key effector cells and targets of autoimmune attacks.[4] In GO development, enhanced TSHR expression is driven by autoimmune and inflammatory processes, paralleling de novo adipogenesis.[11] Compared to healthy donors, TSHR expression was significantly higher in orbital tissues from GO patients (Figure S6A,B, Supporting Information).