Based on our data, we propose that increased pro-inflammatory cytokine signalling parallel to a defective type II IFN response is a key mediator of critical COVID-19 pathophysiology; thereby making (a combination of) specific anti-cytokine monoclonal antibodies (e.g. anti-IL-6) or broad-activity immunomodulatory drugs (e.g. colchicine, azithromycin) interesting candidates for interventional clinical trials. The gene discussed is IL6; the disease is COVID-19.