Good syndrome (GS) is an acquired adult-onset combined immunodeficiency typically characterized by thymoma and hypogammaglobulinemia. Other clinical manifestations include recurrent infections, autoimmunity, and secondary malignancy [1]. However, the spectrum of acquired immunodeficiency observed in patients with thymoma is more diverse and heterogeneous than previously recognized, extending beyond the classic presentation of hypogammaglobulinemia. The impaired expression of autoimmune regulator (AIRE) in thymoma plays a crucial role in the development of immune dysregulation in these patients, given its critical function in central T cell education and autoreactive clone elimination.
