"Interestingly, whole-body size deficits, learning defects and aberrant RAS/ERK signaling are also key features of the NF1 condition in humans, and are all due to a deregulation of the Anaplastic lymphoma Kinase ALK-NF1-RAS/ERK signaling pathway in flies.Pharmacological treatment using a highly-specific ALK inhibitor corrected all these defects in flies and this therapeutic approach was later successfully validated in a preclinical mouse model of NF1 by treating mice with Alectinib, suggesting it represents a promising therapeutic target.