However, a cohort study by Sinha et al. (2020) obtained results that contrasted with these data from the perspective that the hyperinflammatory phenotype of ARDS caused by COVID-19 is associated with higher circulating levels of pro-inflammatory biomarkers such as IL-6, IL-8/CXCL8, and soluble TNFR1 and lower levels of vitamin K-dependent protein C is also related to other factors, and much of the pathogenesis of the disease is not explained by pro-inflammatory biomarkers, especially IL-6 and TFNR1. This evidence concerns the gene TNFRSF1A and acute respiratory distress syndrome.