Given FMRP’s function as an RNA-binding protein that regulates the synthesis of many synaptic plasticity-related proteins (Darnell and Klann, 2013), and altered protein synthesis-dependent synaptic plasticity is a signature phenotype in the Fmr1 KO mice (Huber et al., 2002), it is conceivable that the cognitive deficit observed in Fmr1 KO mice is due to defective transformation of transient learning-induced neuronal activation into lasting memory traces. The gene discussed is FMR1; the disease is Cognitive impairment.