Prior evidences in chronic hepatitis B and hepatitis C virus infections have implicated HLA-E_KLRC/D/K1 signaling in driving T cell dysfunction and supporting viral persistence.29 Moreover, the ICAM1-ITGAL axis has been shown to inhibit T cell immune responses to infections and promote immune evasion for Echinococcus granulosus in mice.30 Collectively, these findings highlight potential targets for further investigation into the pathogenesis and therapeutic interventions for severe bacterial infections. The gene discussed is ITGAL; the disease is chronic hepatitis B virus infection.