Despite there being no differences between ‘clinically defined’ LC and NLC, a trend toward an increase in the transcript levels of the main IFN-I pathway components (IFN-α and IFN-β) was observed among LC participants, suggesting that these IFN-I subtypes may play a key role in the development of LC symptoms [27]. The gene discussed is IFNA2; the disease is laryngotracheoesophageal cleft.