The present findings in the Ts65Dn trisomy mouse model of Down syndrome and the Ube3a maternally-derived mutant mouse model of Angelman syndrome, along with our previous parallel findings in the Fmr1 mutant mouse model of Fragile X syndrome38, support the strategy of therapeutic behavioral interventions using spaced sessions of distributed learning opportunities, to enhance cognitive abilities in neurodevelopmental disorders characterized by intellectual disabilities. This evidence concerns the gene FMR1 and Intellectual disability.