IL4 and COVID-19: We speculate that better adherence to asthmatic treatments during the pandemic [58], the fact that the gene expression of ACE2, TMPRSS2, and furin is not upregulated in asthmatic patients [59], or that the differences in asthma phenotype that were not deeply analyzed across the studies [60], and the inflammatory milieu in asthmatic patients (type 2 cytokines, including IL-4 and IL-13 and accumulation of eosinophils) or the conventional therapeutics for asthma, including inhaled corticosteroids [61] may have conferred a protective effect for asthmatic patients with COVID-19.