From a molecular standpoint, the decreased efficiency of the retino-geniculo-cortical pathway in Fmr1−/y mice must be linked to the impairments of neuron-specific functions such as glutamate/GABA pathways or synaptic transmissions (Davidovic et al., 2011; Doll et al., 2017) due to well described protein deregulation in FXS conditions, such as PSD95, mGlur5, or SNARE complex expression defects (Zhu et al., 2011; Westmark, 2013; Tang et al., 2015; Aloisi et al., 2017). The gene discussed is GRM5; the disease is fragile X syndrome.