Therefore, data from independent studies carried out on different in vitro human models of FXS (Halevy et al., 2015; Telias et al., 2015b), seem to indicate that FMRP loss results in a failure to inactivate the expression of negative regulators of neurogenesis, an idea that is consistent with the role of FMRP as a negative regulator of translation, even though direct protein-mRNA interaction was not demonstrated. The gene discussed is FMR1; the disease is fragile X syndrome.