Altogether these studies show that during acute CoV infection, inflammatory monocyte-macrophages and neutrophils accumulate in the lungs and produce cytokines and chemokines that induce the activation and migration of lymphocytes, including NK cells, to the lungs, where they could be one of the main producers of IFN-γ (148). Under normal conditions, human lung NK cells are typically hyporesponsive but dynamically migrate in and out of pulmonary tissues (83). This supports the hypothesis that during infectious respiratory diseases, an increased recruitment of hyperresponsive NK cells would worsen the festering immunopathology (8). In fact, through Viral-Track scanning of unmapped single-cell RNA-sequencing data, Bost et al. showed that patients with severe COVID-19 exhibited a hyperinflammatory response with an enriched and highly proliferative NK cell compartment (142). High levels of IFN-γ leads to epithelial and endothelial cell apoptosis and vascular leakage, suboptimal T cell response, accumulation of alternatively activated macrophages and altered tissue homeostasis, and ARDS (19), all of which may contribute to COVID-19 disease severity. In summary, the evidence is consistent with the hypothesis that NK cells are involved in the cytokine storm associated with CoV infection and that this hyper-cytokinemia contributes significantly to disease severity via inflammation-mediated lung damage (Figure 1).