Metastasis is the primary cause of death in breast cancer patients as it refractory to current therapies. The first step in metastatic disease occurs when a cell invades surrounding tissue. However, before a cell can invade, its nucleus must become malleable enough to ensure the cell can squeeze through the local tissue matrix. The requirement for nuclear reorganisation at this critical stage provides a unique opportunity to prevent metastasis by targeting the key pathways involved. Heterochromatin Protein 1a (HP1a) maintains the highly condensed portion of the genome and tethers it to the nuclear membrane. We propose the loss of HP1a that is commonly observed in invasive breast tumours, is responsible for the changes in nuclear architecture that lead to increased nuclear malleability in these cells. Therefore, by exploring nuclear remodelling pathways regulated by HP1a, we will reveal potential new drug targets for therapy of metastatic breast disease.