Abstract
The function of histone deacetylase 2 (HDAC2) in transcriptional regulation and its role in oncogenesis have been well established. Here we discuss a transcription-independent HDAC2 pathway controlling cancer-related protein stability via the mouse double minute 2 homolog (MDM2) ubiquitin ligase. In synovial sarcoma, HDAC2 inactivation demonstrates significant therapeutic effect by degradation of the SS18-SSX driver oncoprotein.