Phenotypic plasticity is a new hallmark of cancer which underlies many aspects of cancer evolution, metastasis, and therapy resistance. Breast cancer is the most common and most lethal cancer among women worldwide. Heightened plasticity is thought to underlie the more aggressive subtypes associated with poor prognosis. The molecular basis of this plasticity remains elusive. Bivalent chromatin is defined by the co-occurrence of active-associated trimethyl-lysine 4 on histone H3 (H3K4me3) and repressive-associated trimethyl-lysine 27 on histone H3 (H3K27me3) histone modifications on the same nucleosome. It is a well-defined marker of molecular plasticity in embryonic cells where it poises developmental genes to enable new gene expression programs upon differentiation. We hypothesise that bivalent chromatin may similarly be used by breast cancer cells, facilitating their adaptation and evolution. In breast cancer, bivalency is linked to chemo-resistance and enhanced tumorigenicity, however its dynamics, resolution, and regulation is understudied. This is partly due to the technical challenges distinguishing bone-fide bivalency, where both marks are on the same nucleosome, from allelic or sample heterogeneity where there is a mix of H3K4me3-only and H3K27me3-only mono-nucleosomes. Here, we present a robust ChIP-reChIP protocol to accurately map bivalent chromatin. Using this method, we are generating genome-wide maps of bivalent chromatin in human embryonic stem cells, normal mammary epithelial cells, and a series of breast cancer cell lines. This will enable us to determine how bivalent chromatin primes transcriptional networks of biological and clinical importance while also enhancing our understanding of the fundamental molecular processes driving plasticity in breast cancer.