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Background: Adhesion to extracellular matrix regulates cell survival via integrin engagement and cell spreading. Anoikis is the molecular mechanism of apop-tosis induced by integrin detachment. A role for Bit1 (Bcl-2 inhibitor of transcription 1) has been identified in this process. Bit1 is a mitochondrial protein released into the cytoplasm upon onset of apoptosis where it forms a complex with AES, a small Groucho/transducin-like enhancer of split (TLE) protein and induces caspase-independent apoptosis. AES and TLE proteins are transcriptional co-repressors that play important roles in neurogenesis, segmentation, and sex determination. Bit1-AES complexes may switch off a survival-promoting gene transcription program controlled by TLE. Apoptosis of Bit1/AES transfected cells is inhibited when cells are permitted to attach to fibronectin through the alpha-beta integrin, suggesting that the contribution of the Bit1-AES pathway to anoikis is regulated by integrins.