The reason why the disease is less robust in extremely young animals or humans than in older ones may therefore lie not only in some “cross-immunity” offered by previous infection to “common cold” viruses experienced by children, nor does it lie exclusively in a powerful immune system that, as a result, is not affected by the senescence process; it is probably also affected by an unique ACE2 plasma profile that need to be dissected. Here, ACE2 is linked to infection.