Learning and memory difficulties observed in patients with fragile X syndrome, as well as in a mouse model for the syndrome, are partially due to impaired translational regulation of neuronal mRNAs encoding key molecules for the synaptic structure and function. There has been intense interest in characterizing the mRNAs that are regulated by the fragile X mental retardation protein (FMRP) in the neuronal cell. A large number of candidate FMRP-interacting mRNAs has been identified over the last few years and three models have been described so far to explain the specificity of these interactions. Here, we report our vision on how they could work in the same and/or in different pathways and suggest that the three mechanisms may not be mutually exclusive.