The general objective of our studies is to understand the molecular bases of intellectual disability in Noonan syndrome (NS) and related disorders, which is caused by mutations in genes encoding proteins of the RAS-ERK1/2 signaling pathways. Gene interaction studies in Drosophila showed that developmental defects produced by mutations associated with NS are modulated by RAS-ERK1/2 and JAK/STAT (Janus Kinase / Signal Transducer and Activator of Transcription) signaling. Previous studies indicate that STAT, like RAS-ERK1/2, participates in long-term memory (LTM) formation. Preliminary studies from our laboratory show that genetic manipulation of STAT abolishes the spacing effect (SE) in aversive olfactory conditioning. The SE refers to the enhancement of memory following spaced training sessions (with time intervals between sessions) compared to the same number of training sessions in a massed regime (without such intervals). This effect is reduced in animal models of NS; therefore, we aim to determine the role of STAT in the spacing effect in contextual learning. To this end, we use genetically modified flies with increased or decreased STAT function and analyzed their contribution to memory after massed vs. spaced training. Preliminary results of flies with overexpression of a wild-type allele of STAT showed a distinctive behavioral performance compared with the control genotypes. This study will advance the understanding of the role of STAT in the SE and provide new insights