Furthermore, by disrupting zebrafish orthologs of candidate genes present in large copy number losses identified in HSCR patients, we revealed that HSCR phenotypes can be induced upon loss of the genes: Solute Carrier Family 8 Member A1 (slc8a1), Mitogen-Activated Protein Kinase 8 (mapk8), T-Box Transcription Factor 2 (tbx2), and Ubiquitin Recognition Factor In ER Associated Degradation 1 (ufd1l). This evidence concerns the gene UFD1 and Hirschsprung disease.