Schematic diagram illustrating three techniques to disrupt CTCF-RNA interactions. On the left is an illustration of how the ectopic HA-tagged CTCF swap system works in combination with acute protein degradation of endogenous CTCF. The homozygous miniAID-mClover3 knockin SEM cell lines CTCF AID2/WT and CTCF AID2/dRBR were previously generated [ 11 ]. When added to cell culture, the 5-Ph-IAA auxin analog acts as a ligand to bind to the miniAID tag (fused to endogenous CTCF protein) and OsTIR1(F74G) protein to promote acute protein degradation through ubiquitination by the SCF complex. After 6 h of 5-Ph-IAA treatment, the CTCF HA-tagged WT or CTCF-HA-dRBR ectopic proteins were induced by doxycycline for a total of 18 h of doxycycline and 24 h of 5-Ph-IAA treatment. In the middle is an illustration of transcription inhibition by the natural product, triptolide. Triptolide was added to live cell culture to block the PolII activity and global nascent transcription. On the right is a diagram showing how RNase A was used during the ChIP-seq procedure, either added before (pre-fixation treatment) or after (post-fixation treatment) the chromatin fixation, to degrade global RNAs.