HDAC2 and laryngotracheoesophageal cleft: This phenomenon can be attributed to the ability of low‐concentration butyrate to promote pathways related to cell adhesion and cell–cell junctions, while bacterially derived butyrate inhibits histone deacetylase 2 (HDAC2) and activates M2 macrophage polarization, subsequently inducing the expression of long noncoding RNA H19 in tumor cells, thereby facilitating LC metastasis.