Functionally, COVID-19 patients with the D/D genotype may have an unopposed abundance of angiotension II protein in their blood as a result of the following: increased D allele-mediated excessive ACE expression on one hand and downregulation of ACE2 receptor because of SARS-CoV-2 engagement on the other, thus triggering downstream deleterious effects, the most notable of which is acute lung injury [15]. The gene discussed is ACE; the disease is COVID-19.