The pathogenesis might involve excessive generalized immune response and cytokine storm, direct cytotoxic effect of SARS CoV-2 on pituitary and thyroid cells (9–12), altered activity of deiodinases (especially if the concomitant disease is severe), changes in concentrations of carrier proteins for thyroid hormones, changes of thyroid hormone carriers activity (9), endogenous dopamine release, and non-neoplastic hypercortisolemia (18, 20, 22). Here, TG is linked to adrenal gland hyperfunction.