The proinflammatory cytokines (such as interlukin [IL]-β, TNF-α, IFN-γ) may lead to immune response hyperactivity and uncontrolled systemic inflammatory response.3 Enhanced T-helper (Th1/Th17) immune responses and cytokine pathways involved in severe acute respiratory syndrome (SARS) resemble the immune activation occurring in immune-mediated thyroid diseases.4 ACE-2 and transmembrane protease serine 2 (TMPRSS2) expression are extremely high in the thyroid more than that in the lungs.5 This evidence concerns the gene TMPRSS2 and severe acute respiratory syndrome.