RASopathies are developmental syndromes caused by germline mutations in genes of the RAS/MAPK signalling pathway, commonly associated with variable cognitive impairment. Behavioural studies with animals modelling RASopathies have shown a long-term memory impairment and alterations of the molecular dynamic involved in the spacing effect, but not other defects. Therefore, we considered the necessity to examine other behavioural paradigms, including exploratory activity, contextual recognition memory and learning generalization. These paradigms with freely behaving animals will allow us to test the effect of drugs on the behavioural defects detected. In this study, we used Drosophila to investigate how gain-of-function (CSW-A72S) and wild-type (CSW-WT) alleles of the SHP2 ortholog (CSW) affect learning and memory. Contextual habituation and recognition memory paradigms were used to assess memory specificity and generalization, comparing transgenic lines with parental controls. Our working hypothesis is that hyperactivation of RAS/MAPK signalling in CSW-A72S flies and presumably other molecular mechanisms will affect behavioural performance beside the typically long-term memory impairment. This work will advance the understanding of molecular mechanisms underlying cognitive dysfunction in RASopathies and provide a platform for testing potential therapeutic strategies.