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). The gene discussed is CD40; the disease is COVID-19.