This study indicates that the dysregulation of SALL4, WNT10A, RASAL1, CAMK2B, GADD45B, KLF4, OLR1, CSF3, WIF1, RAMP3, AGER and PRKAG in both sarcoidosis and LC, which could be attributed to common pathological processes such as chronic inflammation, immune imbalance, and aberrant cellular signaling. This evidence concerns the gene AGER and laryngotracheoesophageal cleft.