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Deletion of  Sox2  from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that  Sox2  can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy,  Sox3  can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both  Sox2  and  Sox3  prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of  Sox2  heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency.

Distinct SoxB1 networks are required for naïve and primed pluripotency