This fragment is sufficient to induce apoptosis when it is myristoylated and overexpressed in immortalized cells.[21] The ZU‐5 domain and the DD interact with pro‐apoptotic proteins such as the common neurotrophin receptor, p75, interaction MAGE homolog (NRAGE), and the serine‐threonine death‐associated protein kinase (DAPK).[14a] Most recently, we reported that deletion of netrin‐1 in the adult substantia nigra of mice, mimicking the reduction in netrin‐1 levels in PD patient brains, induces DCC cleavage and dopamine neuronal loss, resulting in motor deficits. The gene discussed is MAGED1; the disease is Parkinson disease.