Finally, we found that abnormalities in nAChR function and XIIMN firing properties identified at P10–P12 are associated with altered respiratory-related tongue muscle control in vivo, which is a novel finding that elucidates important mechanisms behind how DNE leads to a behavioral vulnerability at a critical period of respiratory system development, a phenotype that nicely models key aspects of the pathogenesis of SIDS. The gene discussed is CHRNA4; the disease is sudden infant death syndrome.