Even without an AAT deficiency, the AAT response may be insufficient in critically ill COVID-19 patients [87,88], perhaps due to the AAT heterozygosity (e.g., the protease inhibitor (Pi)MZ) that results in a suboptimal increase in AAT levels [6] or to the oxidation of normal AAT in highly oxidative states such as severe COVID-19, causing loss of its serpin activity [89] or inducing its polymerization [9,90]. The gene discussed is SERPINA1; the disease is COVID-19.