We have proposed a "switching concept" for the neurogenesis of ventilatory activity. Eupnea reflects the output of a pontomedullary neuronal circuit, whereas gasping is generated by medullary pacemaker mechanisms. Pontile mechanisms, then, are hypothesized to play a fundamental role in the neurogenesis of eupnea. If pontile mechanisms do play such a critical role, several criteria must be fulfilled. First, perturbations of pontile regions must alter eupnea under all experimental conditions. Second, neuronal activities that are consistent with generating the eupneic rhythm must be recorded in pons. Finally, medullary mechanisms alone cannot fully explain the neurogenesis of eupnea. Evidence from previous studies that support the validity of these criteria is presented herein. We conclude that pontile mechanisms play a critical role in the neurogenesis of eupnea.