Interestingly, the herpesvirus protein ICP0, which shares its PML NB-targeting capability with that of E4-ORF3, functions as a STUbL that preferentially ubiquitinates poly-SUMOylated PML during herpesvirus infection as a mechanism to inhibit the antiviral activities of PML (38). This evidence concerns the gene PML and Herpesviridae infectious disease.