NOS1 and Hirschsprung disease: Caveolin-1 (Cav-1) regulates the functions of different NOS isoforms, and Nakamura [58] previously found a lower expression level of Cav-1 in the colon of patients with HSCR, which led them to speculate that reduced Cav-1 expression may lead to excessive activation of iNOS, consequently leading to epithelial damage and thus increasing the susceptibility of HSCR to HAEC.