In this regard ANP32E may act to ‘lock in’ a defined chromatin state, and when tumor cells transition to later stages of cancer progression, ANP32E becomes downregulated, leading to increased chromatin accessibility at a defined set of gene regulatory regions, including sites where H3K27ac and H2A.Z are enriched, enhancer elements, and FOXA1 binding sites. The gene discussed is FOXA1; the disease is cancer.