FOXM1 is expressed in undifferentiated hESCs with peak levels at G2/M phase.
FOXM1 depletion causes mitotic defect and delays G2/M progression in hESCs.
FOXM1 downregulation does not induce rapid exit of undifferentiated state in hESCs.
FOXM1 depletion sensitizes hESCs to oxidative stress.
Genomic binding profile of FOXM1 in hESCs differs substantially from cancer cells.