This may have resulted from corticosteroid properties, including inhibition of CD4+ and CD8+ T-cell proliferation, suppression of cytokine production (e.g., IFN-γ, IL-2), impairment of dendritic cell differentiation and maturation, and induction of apoptosis, all of which may attenuate ICI-driven thyroid autoimmunity [22]. The gene discussed is IFNG; the disease is autoimmune thyroid disease.