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Remarkable progress in elucidating the molecular pathogenesis and neurobehavioral features of fragile X syndrome (FXS) since the discovery of the FMR1 gene in 1991 has paved the way for novel therapeutic targets in FXS (reviewed in [1]. FXS is caused by a mutation in the Fragile X Mental Retardation 1 gene (FMR1) that typically expands the normal 30-45 CCG triplet nucleotide repeats to >200, termed the full-mutation (Figure 1).

Challenges in Translating Therapeutic Frontiers in Clinical Trials: Where Are We Now and What's Next?