In particular, with regard to Wnt2B, a recent study demonstrated that, in LC, DDX56 (DEAD-Box Helicase 56) can increase the transcription of the target gene Wnt2B through the degradation of primary miR-378a [41]; additionally, RPPH1 (ribonuclease P RNA component H1), a long non-coding RNA associated with NSCLC progression and cisplatin resistance, is recognized to stimulate the Wnt pathway by elevating Wnt2B expression via the RPPH1/miR-326/Wnt2B axis [42]. This evidence concerns the gene ENSG00000259001 and laryngotracheoesophageal cleft.