Human embryonic stem cells (hESCs) are exquisitely sensitive to WNT ligands that rapidly cause differentiation. Therefore, hESC self-renewal requires robust mechanisms to keep the cells in a WNT-inactive, but–responsive state. How they achieve this is largely unknown. We explored the role of transcriptional regulators of WNT signaling, the TCF/LEFs. As in mouse ESCs, TCF7L1 is the predominant family member in hESCs. Genome-wide, it binds a gene cohort involved in primitive streak formation at gastrulation including NODAL, BMP4 and WNT3. Comparing TCF7L1-bound sites with those bound by the WNT signaling effector, β-CATENIN, indicates that TCF7L1 acts largely on the WNT signaling pathway and not other processes. TCF7L1 overlaps less with the pluripotency regulators OCT4 and NANOG than in mouse ESCs. Gain- and loss-of-function studies indicate that TCF7L1 suppresses gene cohorts expressed in the primitive streak. Interestingly, we also find that BMP4, another driver of hESC differentiation, down-regulates TCF7L1, providing a mechanism of BMP and WNT pathway intersection. Together our studies indicate that TCF7L1 plays a major role in maintaining hESCs pluripotency, studies that have implications for human development during gastrulation.