Whenever you see a "STAT1" ChIP-Seq peak at the CTCF loop anchor (by Hi-C), you also observe the STAT1 peak at the other anchor of the same CTCF loop:

Hi-C loops 

The explanation proposed by the authors:

"While ChIP-seq was not designed to detect chromatin interactions, the formaldehyde treatment in the ChIP-seq protocol cross-links proteins with each other and with DNA. Consequently, also regions that are not directly bound by the targeted TF but interact with the binding site via chromatin looping are coimmunoprecipitated and sequenced. This produces minor ChIP-seq signals at loop anchor regions close to the directly bound site."

1. Dimerization of "STAT1", 
2. CTCF-"STAT1" protein complex,
3. "STAT1" complex with some other factors that co-localize with loops,
4. Genome duplications,
5. Mutations in cancer,
6. Problems with sample preparation, e.g. binding of antibodies to all open chromatin regions. 

ATAC-Seq

Hsu et al. 2018

paired-end sequencing and mapping

"ecDNA displayed a significant deficit in the number of long fragments (more than 1,200 bp) from ATAC-seq and MNase-seq, indicative of compacted nucleosomal arrays, and a significantly increased number of ATAC-seq peaks, which suggests that the ecDNA chromatin landscape is more accessible than chrDNA, because its nucleosomal organization is less compacted."

Red-C for RNA-DNA high-throughput assay

Gavrilov, Zharikova, Mironov, Galitsyna, paper in review

Red-C for RNA-DNA high-throughput assay

Typical mistake is that you don't consider that coverages for RNA and DNA are separate: