As summarized in Table 1, mouse models for Costello Syndrome (CS), Neurofibromatosis I (NF1), Noonan Syndrome (NS), and Legius Syndrome show similar phenotypes including hyperactivity of the RAS-ERK pathway, learning deficits in the water maze, and impaired synaptic plasticity, which confirm the widespread observation of overlapping disease manifestations across patients with different RASopathies. This evidence concerns the gene MAPK1 and Noonan syndrome.