This is partially attributable to the polygenetic causes of HSCR, including mutations in several common genes: proto-oncogene RET (RET), glial cell line derived neurotrophic factor (GDNF), endothelin B-receptor (ETB), endothelin-3 (ET-3), SOX10, endothelin converting enzyme-1 (ECE-1), neurturin (NTN), and Smad interacting protein 1 (SIP1) genes [12, 13]. This evidence concerns the gene ECE1 and Hirschsprung disease.