The cell cycle has been a central focal point for cancer research since the Nobel prize winning discoveries of Hartwell, Nurse and Hunt in the nineteen seventies and eighties. Recent clinical success with inhibitors of cyclin dependent kinases (CDK) 4/6 has again put the cell cycle and its role in cancer into sharp research focus. 2 CDK4/6 inhibitors target the cyclin dependent kinases (CDKs), a group of proteins that together with their binding partners - the cyclins, are responsible for cell cycle phase transitions. These distinct phases are commonly referred to as G1, S, G2 and M. Whilst a wealth of single cancer cell RNA-sequencing data exists, cells are typically FACS sorted into cell cycle phases prior to sequencing. This means that we not only miss the very phase transition genes we are interested in studying, but also introduce a batch effect into the data that makes it difficult to decouple gene expression differences between the cell cycle phases from technical artifacts. We aim to understand differences in oncogenic signaling between cell cycle phases in breast cancer subtypes, how cell cycle activity is influenced by cellular plasticity and the tumour microenvironment (TME) and if a gene signature representing the cell cycle can be brought to the stage of routine clinical implementation.