This putative “cytokine storm” pathology associated with coronaviruses is also supported by experimental SARS-CoV models, one of which showed that the severity of ALI was accompanied by an elevated expression of inflammation-related genes rather than increased viral titers. In another case, the ablation of IFN-α/β receptor or the depletion of inflammatory monocytes/macrophages caused a marked rise in the survival rate of coronaviruses host without a change in viral load [19,20]. Both situations suggest a potential amplifying mechanism involved in CoV-induced ALI/ARDS regardless of the viral load. If a similar pathology also exists in COVID-19, the attenuation of the cytokine storm by targeting several key steps in the process could bring about improved outcomes.