Notably, the kinin-kallikrein system, implicated in the pathophysiology of COVID-19 by Jakwerth et al. [33], parallels our observations of a robust antiviral state mediated by ISGs, suggesting a universal epithelial response to viral threats that includes both rapid ISG upregulation and modulation of receptor-mediated signaling pathways. The gene discussed is KLK4; the disease is COVID-19.