Several hypotheses have been proposed to explain why children are protected from more severe outcomes with COVID-19, including differences in expression of angiotensin-converting enzyme 2 (ACE2), the receptor for viral entry, resulting in lower viral loads; presence of antibodies to common cold coronaviruses that might provide partial protection; and a more robust innate response early in the course of infection that mitigates against a vigorous adaptive response (3, 4). Here, ACE2 is linked to infection.