Changes in the innate and adaptive arms of the immune system, a blunted IFN-1 response to control and clear viral infection, and reduced angiotensin-converting enzyme 2 (ACE2) activity in the lungs contribute to increased release of pro-inflammatory cytokines and chemokines, thus promoting inflammation, vascular permeability, and poor outcomes in aged COVID-19 patients (Fajgenbaum and June, 2020; Rydyznski Moderbacher et al., 2020). Here, ACE2 is linked to COVID-19.