Further, histone H3 lysine 27 acetylation (H3K27ac) was found to be altered during acquisition or resistance to anaplastic lymphoma kinase inhibitors in patients with ALK (anaplastic lymphoma receptor tyrosine kinase) fusion-positive LC; its decreased levels correlated with downregulation of tumor-suppressive miR-34a and miR-449a and increased proliferation [116] (Table 2). This evidence concerns the gene ALK and laryngotracheoesophageal cleft.