As mentioned in section 4, DMXAA could only recognize murine STING.[90] Recently, it was demonstrated that DMXAA functions as a partial STING agonist, performing a more suppressive effect on the STING‐IRF3 axis than on the NF‐κB axis.[60] Since NC NF‐κB activation through STING has been linked to immunosuppressive effects and mediating tumor growth, this could potentially explain the lack of effectiveness observed in clinical trials. The gene discussed is IRF3; the disease is neoplasm.