To demonstrate the involvement of PKM1/PKM2 in this process, particularly in the severe form of HSCR, which showed significant association with PKM1 expression, we employed morpholinos targeting the splicing sites of PKM gene to alter the levels of PKM1 (Intron 8/ Exon 9) and PKM2 (Exon 10/Intron 10), respectively, in control- and HSCR-ENCCs. The gene discussed is PKM; the disease is Hirschsprung disease.