Pulmonary fibrous strips and fibrosis were reported in 17% of COVID-19 patients.171 The hallmark in the pathophysiology of ARDS is the increase in permeability of the alveolar-capillary epithelial barrier that allows protein-rich fluid to enter the alveoli leading to pulmonary edema, hypoxemia, and consequent release of proinflammatory cytokines such as IL-1β, IL-6, IL-8, and TNF-α.172 Similar pathological changes of DAD in the lung are identified in COVID‐19 associated ARDS and the typical ARDS.173. This evidence concerns the gene IL6 and acute respiratory distress syndrome.