While in the late phase of infection, damaged DNA (i.e., oxidized mitochondrial DNA) potentially activates the cGAS-STING pathway as a result of the micronuclei and syncytia formation in the infected cells [73], leading to excessive release of IFN-β and substantial cytokine storm phenomenon during IRF-3 and NFκB activation [70, 72, 74]. The gene discussed is IRF3; the disease is infection.