MAGEL2 and Prader-Willi syndrome: This speculation is supported by experiments on genetically engineered mouse models of PWS; Magel2-deficient mice have shown defective neuropeptide secretion ability (Chen et al., 2020) and dopaminergic dysfunction (Luck et al., 2016), and Ndn-deficient mice have shown abnormal noradrenergic excitability (Wu et al., 2020).