FMR1 and fragile X syndrome: Studies in human FXS cell lines aiming to reactivate FMR1 by either changing repressive Histone modifications (Kumari and Usdin, 2016; Dolskiy et al., 2017) or decreasing CpG methylation (Chiurazzi et al., 1998; Coffee et al., 2002; Tabolacci et al., 2005, 2016a), suggest that DNA methylation is the primary cause for gene inactivity, while repressive Histone methylations have a supportive function.