Mechanistically, researchers are attempting to address the question of how CGG expansion leads to de novo methylation of the 5′-UTR of FMR1 by taking advantage of FXS hESCs which, unlike the somatic cells of patients and patient-derived iPSCs, provide an unusual opportunity to uncouple CGG expansion and heterochromatin induction in a developmentally regulated context. Here, FMR1 is linked to fragile X syndrome.