Menkes disease is an X-linked recessive defect in which the essential trace element copper cannot be properly metabolized by the gut, leading to brain damage and early death. Bahadorani and colleagues show that inhibiting the Drosophila version of the copper exporter gene that is mutated in Menkes patients causes a phenotype with similarities to the human disorder, with severe effects on brain development. This model provides a simple, fast and cheap way of identifying novel modifiers of the disease, and hence new treatment options.

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