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Interestingly, we demonstrated an increased binding of β-catenin to FOXO1 in PELO-mutant ESCs cultured under differentiation condition that could explain, on one side, the nuclear accumulation of FOXO1 protein and hence persistent pluripotency of PELO-mutant ESCs, and on the other side, the dysregulated transcriptional activity of β-catenin/TCF and therefore attenuated PELO-null ESCs self-renewal. Taken together, our results strongly suggest that PELO deletion averts ESCs differentiation through promoting FOXO1/β-catenin binding with sub