Since the fine-tuned immune response is vital in determining the outcome of the SARS-CoV-2 infection [32], we can hypothesize that decreased serum concentrations of SEMA3A in COVID-19 patients and its negative correlation with disease severity might result in the lack of anti-inflammatory and immunosuppressive effects of SEMA3A, which might lead to an uncontrolled inflammatory cascade. This evidence concerns the gene SEMA3A and COVID-19.