Although endothelial dysfunction in children with OSA also improves following AT,12 it is important to note that AT is much less effective at eradicating OSA than previously anticipated, particularly in the context of concurrent obesity.13,14 In fact, six (33%) of the 18 children in the present cohort had evidence of residual OSA post-AT of moderate severity, and OSA was only effectively cured with AT in two (11%) of the 18 children.4 Thus, even partial improvements in the severity of OSA yield returns of altered LF/HF to within normal levels. Stratification to post-AT apnea-hypopnea index (AHI) >5/h and post-AT AHI >5/h groups further revealed significant reductions in LF/HF in stages N3 and rapid-eye-movement sleep in children with post-AT AHI <5/h but absence of any significant changes in LF/HF when post-AT AHI remained >5/h. These findings support the notion that a threshold for the magnitude of respiratory disturbance may be present in children and that such a threshold likely revolves around an AHI of 5/h, whereby the tonic sympathetic activation elicited by the presence of OSA appears to be manifest only after a particular level of disease severity is reached. Before seeking reassurance in such deductions, however, we also should point out that elevations in systemic BP may occur in children with primary snoring15 (ie, in the presence of AHI <1/h). Therefore, the normalization of LF/HFs reported by Muzumdar and colleagues4 may be inherent to the small size of the cohort in the study, which does not allow for ruling out the presence of a β error.