Curiously, we were unable to co-IP RUNX2 and PR from breast cancer cell whole cell lysates or detect them as co-associated factors at PRE sites by ChIP assays, suggesting that these factors function in the same pathway but may interact indirectly or may associate transiently or successively via binding to separate or distant sites in chromatin (a topic for further study). This evidence concerns the gene RUNX2 and breast carcinoma.