I’m overexpressing a fusion gene PML-RARA with the RARA moiety containing DNA binding domain in a leukemia cell line. After binding to RARA response elements in target genes, PML-RARA would recruit corepressors like HDAC and lead to transcription repression, which means PML-RARA overexpression should bring about less accessible chromatin of target genes compared with control group. However, when I induced PML-RARA expression in early time points I found the mRNA expression examined by RNA-seq was downregulated as expected, while the chromatin status detected by ATAC-seq remained more accessible than control group. I’m confused with the discrepancy between chromatin status and gene expression. I’m wondering would the chromatin keep opening for the occupancy of inducible expression of transcription factor? Or will the chromatin status be dynamic like more accessible at early times and finally less accessible due to recruitment of corepressors?