Using the cell lines that model hormone-responsive (ECC1), moderately differentiated/low PR (Ishikawa H), and poorly differentiated/no PR (Hec50co) endometrial cancers, we treated cells with DMSO vehicle control, the PR antagonist (RU486) combined with the MAP kinase inhibitor (PD0325901), the HDAC inhibitor (LBH589), or the hypomethylating agent (5-aza-dC). This evidence concerns the gene HDAC9 and endometrial cancer.