Because HMGB1 was similarly accumulated in patients with COVID-19 [184], these TN/RBM-reactive mAbs might simultaneously block harmful TN/HMGB1 interaction and resultant immunosuppression, and suppress possible SARS-CoV-2/ACE2 interaction to inhibit GM-CSF production in patients with COVID-19 and other lethal infections [71]. The gene discussed is CSF2; the disease is COVID-19.