Epithelial to Mesenchymal Transition, the process whereby epithelial cells transition into motile mesenchymal cells is an important process in development, and is associated with cancer metastasis. In Drosophila melanogaster an EMT like event occurs during the eversion of the wing disc. Cells of the peripodial epithelium lose apico-basal polarity, cell-cell junctions break down and the cells take on an invasive, migratory phenotype. In an RNAi screen for EMT factors we identified the secreted axon guidance factor Netrin-A. We find that Netrin-A, and its paralog Netrin-B, promote DE-Cadherin breakdown in the peripodial epithelium, by downregulating its receptor Frazzled (Manhire-Heath et al, Nat. Comms. 2013, 4:2790). To find EMT factors that genetically interact with Netrins we rescreened the hits from the primary screen in a genetic background lacking netrin-B. netrin-B mutants are viable and fertile, but loss of netrin-B enhances the penetrance of eversion defects of other genes, such as netrin-A. The screen identified two gene candidates, the polycomb group (PcG) gene sex combs extra (Sce) and phosphoinositide-3-kinase (Pi3K92E). PcG genes are epigenetic regulators that target histones, and are well known for their ability to suppress homeotic genes. Pi3K92E catalyses the production of phosphatidylinositol-3,4,5 triphosphate (PIP3), which can recruit numerous signalling proteins and thereby regulate cell survival, cell migration and cell death. Knockdown of other PcG genes also caused eversion failure defects, consistent with these proteins functioning in complexes. Using an in vitro overnight culture assay we have also confirmed that RNAi to Sce and Pi3K92E disrupts the eversion process. Future work will characterise the role of PcG genes and Pi3K92E in controlling epithelial breakdown and acquisition of motility, and investigate the interaction between these genes and the Jun-Kinase and the Netrin/Frazzled pathways, which are known to regulate eversion.