Interestingly, in a model of Noonan’s syndrome in which the protein tyrosine phosphatase SHP2 is mutated, the temporal profile of ERK1/2 activation in response to a training trial is prolonged, and the pattern of repeated-trial training permissive for LTM formation in wildtype flies results in impaired LTM in SHP2 mutant flies. This evidence concerns the gene PTPN11 and Noonan syndrome.