Specifically, during ZIKV infection, SUMOylation of NS5 decreases its ubiquitin-mediated degradation and promotes its interaction with the signal transducer and activator of transcription-2 (STAT2) protein, which disrupts the host antiviral promyelocytic leukemia (PML)-STAT2 nuclear bodies (NBs) and leads to the degradation of PML [76]. The gene discussed is RAF1; the disease is Zika virus infectious disease.