Because a subset of severe COVID-19 infections have a delayed onset of respiratory distress despite the severity of hypoxemia that clearly differs from classic ARDS but principally involves a catastrophic microvascular injury and thrombosis [35–37], it might be relevant to carefully evaluate the impact of targeting the mitochondrial ROS/CRAC/IL-6 signaling cascade in the respiratory, inflammatory, and survival outcomes during the “typical” and “atypical” presentation of ARDS in COVID-19 patients. The gene discussed is IL6; the disease is COVID-19.