These findings are consistent with earlier reports that YAP/TAZ signaling supports CSC populations and drives drug resistance in breast, bladder, and glioblastoma cancers,33–35 and that YAP regulates SOX2 and Nanog, reinforcing its central role in tumor plasticity.35 Our work presents initial evidence that TEAD2 binds to the OCT4 promoter, a result that remains to be validated with additional experimental approaches despite its potential significance. Here, POU5F1 is linked to neoplasm.