In many cancers unchecked proliferation is driven by inappropriate activity of signalling pathways, such as the Notch pathway. Activation of Notch results directly in changes in gene expression and the consequences differ according to the cell context. We are investigating the mechanisms that underly these different outcomes and the factors that influence whether Notch promotes growth or proliferation. We use Drosophila as our primary model, due to the powerful genetics and small genome size. As ~80% of human disease genes have orthologues in Drosophila our research with this tractable model is able to identify genes of relevance to human cancers that we subsequently study in human cells.