To better understand the response to progestin in endometrial cancer cells, we have studied the genomic binding of ER and PR, the global gene expression changes and the state of chromatin by ATACseq as well as the genomic interactions by Hi-C in Ishikawa cells exposed to progestin or estrogen, and also in cells exposed to progestin after a period of estradiol pretreatment. The gene discussed is ESR1; the disease is endometrial cancer.