FMR1 and fragile X syndrome: In addition, JNK activity is upregulated in synapses of Fmr1 knockout mice, and inhibition of JNK with SP600125 decreased elevated postsynaptic protein synthesis in these mice, suggesting that JNK could be a key signaling downstream of mGluR in regulating FMRP-dependent protein synthesis and may provide a strategy to restore the deficits in fragile X syndrome (Schmit et al., 2013).