The development of ARDS in the context of SARS-CoV-2 is thought to occur through either the virus’s direct invasions on respiratory epithelial cells or through an amplified immune response (3) resulting in the overproduction of cytokines such as IL-10 and TNF-α as well as increased levels of neutrophils, CRP, and NLR, while lymphocyte count decreases (4–7). This evidence concerns the gene TNF and acute respiratory distress syndrome.