TP53 and laryngotracheoesophageal cleft: According to the existing literature, LC and IPF share the following pathogenetic mechanisms in terms of their development: genetic alterations including micro-satellite instability, loss of gene heterozygosity and gene mutations including those of p53; alteration of epigenetics; abnormal expression of microRNAs; cellular and molecular aberrances such as an altered response to regulatory signals and reduced cell-to-cell communication; and activation of specific signaling transduction pathways19–22.