Cell competition is an important surveillance mechanism that measures relative cell fitness in a tissue during development and homeostasis, and is critical for the removal of aberrant cells that may lead to cancer. Fitter cells (winner cells) recognize and eliminate less fit cells (loser cells), which would otherwise survive in a homozygous (all mutant) tissue. Cell competition was initially discovered in Drosophila epithelial tissues, but also occurs in mammalian systems. One type of cell competition involves the cell polarity tumour suppressors genes, scribbled (scrib), disc large (dlg) and lethal giant larvae (lgl), mutation of which in a whole epithelial tissue context result in neoplastic tumours, however when surrounded by wild-type cells the mutant cells have a loser fate in most tissue contexts. In Drosophila epithelial tissues, death of scrib mutant loser cells occurs through a Jun-kinase (JNK)-dependent mechanism that depends upon the surrounding wild-type cells. JNK signalling leads to the transcriptional upregulation and secretion of the inflammatory cytokine, Upd (IL6 ortholog), that activates Jak-Stat signalling in surrounding wild-type cells enabling their compensatory proliferation. Additionally, other signalling pathways are deregulated in scrib mutant cells, including the receptor tyrosine kinase (RTK) EGFR-Ras pathway. However, in scrib mutant cells, the membrane receptor phosphatase, PTP10D, is activated by interaction with a membrane protein, Sas, on the adjacent wild-type cells, and leads to the downregulation of EGFR-Ras signalling. We have evidence that the cytoplasmic phosphatase, PTP61F, also acts in scrib mutant cells to promote their elimination, potentially through downregulation of EGFR-Ras as well as Jak-Stat signalling. Whether these two phosphatases work together and whether they are also involved in cell competition in mammalian cell systems are important questions that we are addressing.