Decline in a number of CD4+ and CD8+ T cells due to either direct attack from SARS-CoV-2 through the spike (S) protein binding with a receptor on T cell [4–7] or induced cellular apoptosis and the subsequent decline in the type I interferons, especially interferon-gamma (IFN-γ) [4, 8, 9], as well as the T cell exhaustion marked by the increased expression of programmed death 1 (PD-1) indicate the state of immunosuppression in COVID-19 patients [4, 10]. The gene discussed is CD8A; the disease is COVID-19.