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). This evidence concerns the gene SOAT1 and laryngotracheoesophageal cleft.