TP53 and laryngotracheoesophageal cleft: As an additional example, miR-34a involved in p53-signalling was found to induce apoptosis in LC [73]; miR-197-5p, miR-93-5p, miR-378a-3p and miR-98-5p downregulate the expression of FUS1/TUSC2 [74], a tumor suppressor gene located on Chr.3p21.3 which is frequently hit by heterozygous (LOH) and homozygous deletions in both small (SCLC) and non-small cell lung cancers (NSCLC) [75]; oncomiR-1 was found to be upregulated in LC and to target critical genes involved in proliferation and tumor angiogenesis [76] and overall in pathogenesis of LC [77].