DYRK1A protein elevation emerges as a key driver of the characteristic enlarged brain phenotype in fragile X syndrome, based on fruit fly modeling that revealed this kinase's role in abnormal neural growth patterns. The research pinpoints a molecular mechanism underlying macrocephaly, a common but poorly understood feature affecting many individuals with this inherited intellectual disability condition. This finding bridges a critical gap in fragile X pathophysiology, as previous research largely focused on synaptic dysfunction and protein synthesis defects rather than gross anatomical changes. The DYRK1A pathway represents a potentially actionable target, particularly relevant given existing small molecule inhibitors of this kinase already in development for other neurological conditions. However, the fruit fly model, while genetically tractable, may not fully recapitulate human brain development complexities. The work also raises questions about whether similar mechanisms drive macrocephaly in other autism spectrum disorders, where enlarged brain volume frequently occurs. For families affected by fragile X syndrome, this research suggests brain overgrowth isn't merely a secondary consequence but involves specific molecular pathways that could theoretically be modulated, though clinical applications remain distant.