Genes described to influence latency included Xpb, Paf1c, and Ccnt1. HDAC inhibitors have described latency reversal potential. We measured total transcription in cells treated with HDAC inhibitors SAHA or Romidepsin to understand molecular mechanisms underlying latency reversal involving HDACi. Cells treated with HDACi experienced an imprinting switch marked by activation of PEG10. HDACi with SAHA or Romidepsin resulted in silencing of Brpf3, Echdc2, and Gtf2ird2b. A gene product encoded by Cttnbp2nl was activated during latency reversal associated with chemical HDACi.