More specifically, the overexpression of PML-VI augmented the production of IFNβ in U373-MG or HeLa cells stimulated by double RNA or virus infection, and this augmentation was attributed to the ability of PML-VI to recruit Pin1 to PML NBs, and thereby prevent the degradation of phosphorylated IRF3 [40]. The gene discussed is IRF3; the disease is viral infectious disease.