Myosins are actin-based molecular motor that are involved in various cellular processes including cell migration and endocytosis. More recently, Myosin VI has been characterised in the nucleus where it has a direct interaction with DNA that is critical for RNA polymerase II transcription. Along with this interaction it has also been shown that myosin VI stabilises p53 allowing DNA repair to occur before the cell cycle continues. However, very little is known about how Myosin VI may function in the DNA damage response. We have found cisplatin-induced DNA damage causes a large increase in the nuclear localisation of myosin VI and we wish to understand the reason for this recruitment. We have begun to understand that myosin VI is required for a normal response to DNA damage by analysing the global changes of chromosome arrangement and histone modifications. These chromatin markers are directly or indirectly linked with the DNA damage response, and the work presented here describes how myosin VI may be involved in not only signalling but also repair factories themselves. By using techniques such as high content screening, co-localisation studies and clustering analysis we are beginning to characterise a new role for myosin VI within the nucleus.