There are multiple mechanisms by which thyroid dysfunction may occur in the setting of SARS-CoV-2 infection including lymphocytic proliferation of the thyroid and via a “cytokine storm” induced by the proinflammatory state of COVID-19.7 The thyroid gland has a relatively high concentration of angiotensin-converting enzyme 2 receptors, which facilitate entry of the virus into cells and may lead to direct thyroid infection.8 These mechanisms are especially relevant since even mild elevation in thyroid hormone in the setting of COVID-19 is linked to increased mortality.4 Here, TG is linked to COVID-19.