For instance, Colak et al., who employed two FXS hESC lines with expansions exceeding 400 CGGs, claimed that hybridization of the mutant mRNA to the promoter and the 5′ flanking region of FMR1 elicits silencing by inducing a change from active (H3K4me2) to repressive (H3K9me2) histone modifications during neural differentiation [21]. The gene discussed is FMR1; the disease is fragile X syndrome.