Both PML and ZBTB16 originally captured attention as translocations with the retinoic acid receptor locus in acute PML patients18,19. Reports by us and others have identified that ZBTB16 modulates inflammatory and antiviral immune responses as a transcription factor by directly inducing gene expression via its C-terminal Krüppel-type zinc-fingers and indirectly by recruiting other factors via its N-terminal BTB/POZ and RD2 domains20–22.
