Reanalysis of ChIP-sequencing data from the hormone-sensitive breast cancer cell line MCF7 (GSE68359)13 revealed that cotreatment with E2 and natural P4, but not E2 alone or with synthetic P4 (R5020), induced the co-occupancy of ERα, PR, and p300 histone acetyltransferase at the promoters of cholesterol biosynthesis genes (Supplementary Fig. 7d). This evidence concerns the gene ESR1 and breast carcinoma.