Neurofibromatosis type I (NF1), caused by the mutation in theNF1gene, is characterized by multiple pathological symptoms. Importantly, ∼50% of NF1 patients also suffer learning difficulty. Although downstream pathways are well studied, regulation of theNF1-encoded neurofibromin protein is less clear. Here, we focused on the pathophysiology ofDrosophila NF1mutants in synaptic growth at neuromuscular junctions. Our analysis suggests that theDrosophilaneurofibromin protein NF1 is required to constrain synaptic growth and transmission. NF1 functions downstream of theDrosophilafocal adhesion kinase (FAK) Fak56 and physically interacts with Fak56. The N-terminal region of NF1 mediates the interaction with Fak56 and is required for the signaling activity and presynaptic localization of NF1. In presynapses, NF1 acts via the cAMP pathway, but independent of its GAP activity, to restrain synaptic growth. Thus, presynaptic FAK signaling may be disrupted, causing abnormal synaptic growth and transmission in the NF1 genetic disorder.