This model revealed that gene expression and protein levels of complement activation, proinflammatory response, JAK-STAT, IL-6, IL-6-JAK-STAT3, IFNβ and IFNγ signaling pathways during acute infection were among the top predictors for the development of LC (Extended Data Fig. 4e,f). The gene discussed is STAT3; the disease is laryngotracheoesophageal cleft.