Taken together, results from the current and previous studies, it is likely that XO-dependent ROS mediates imbalance between HIF-1 and HIF-2 via Nox2 and calpain activation, which leads to further long-lasting oxidative stress during IH that results in autonomic morbidities as summarized in Fig. 7. The gene discussed is HIF1A; the disease is isolated hemihyperplasia.