Along with hyperinflammation in severe COVID-19, there is overwhelming evidence in the literature pointing towards cytotoxic cell immunosuppression due to upregulation of immune exhaustion markers (PD-1, TIGIT, Tim-3, CTLA-4) as an alternative mechanism to severe disease pathogenesis (6, 40, 53–56). The gene discussed is HAVCR2; the disease is COVID-19.