Therefore, associations between STAT1 and T-cell receptors (e.g., CD38, CD40, CD48, CD68) in the mild-severe disease state, may suggest a more efficient role in the immune response to viral infections during mild disease state and higher STAT1 activation in severe disease state contributing to the cytokine storm and hyperinflammation that are characteristic of severe COVID-19 (Hadjadj et al., 2020). This evidence concerns the gene CD68 and viral infectious disease.