Moreover, as a functional validation of a transcriptionally active ERα in the stressed or H3K27me3 pathway-inhibited explants, we demonstrate that both anisomycin and GSK-126 treatment upregulate ERα downstream targets, the progesterone receptor (PGR) and GREB1 in PDEC-BC (Fig. 6c). The gene discussed is GREB1; the disease is breast cancer.