Since null mutations in the genes encoding endothelin-3-endothelin receptor B (EDNRB) are responsible for a subset of HSCR patients [103], Fattahi et al. [15] used hESCs-derived EDNRB−/− ENC precursors as a HSCR model to screen and identify compounds that could rescue the migration defects associated with HSCR. Here, EDN3 is linked to Hirschsprung disease.