A convincing body of evidence now exists that obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular morbidity and mortality [1–3]. OSAS has been specifically associated with hypertension [4], myocardial infarctions [2], stroke [5], and congestive heart failure [6]. Apneic episodes and arousals cause surges in sympathetic tone with the release of vasoactive mediators including catecholamines [7]. Intermittent hypoxia leads to hypoxic vasoconstriction and hypoxia reperfusion oxidative stresses [8]. These metabolic stresses result in a systemic inflammatory response and vascular remodeling. Because treatment of sleep apnea is believed to prevent these complications, it is important that providers of sleep medicine verify effectiveness of treatment, including the ability of patients to comply with prescribed therapy. Commonly employed measures of adherence to therapy include the patient's self-reported history and selfreported change in Epworth Sleepiness Scale or other subjective symptom scales. Such historical self-reports are frequently unreliable. Recent experience has shown that continuous positive airway pressure (CPAP) devices capable of recording the duration and frequency of use provide the best available objective data regarding adherence to CPAP therapy. These data are helpful in explaining symptomatic response to therapy, an important outcome of treatment. However, they are in reality surrogate markers for the long-term outcomes we are interested in knowing. The clinician and patient need to know the impact that the prescribed treatment has had on reducing risk for adverse events such as heart disease and stroke. In their article on nuclear factor-KB (NF-KB) in this journal, Htoo et al. [9] may have provided us a first step toward a new measure of the effectiveness of OSAS therapy in reducing cardiovascular risk. Htoo et al. [9] report their investigation of a potential new surrogate marker that is closely related to systemic inflammation, a probable causative link to cardiovascular disease promotion. There are two very interesting findings in the paper by Htoo et al. [9]. The first is a direct correlation between neutrophil NF-KB activity with indices of apnea severity. The second finding was demonstrated in a subgroup of patients with severe apnea who received CPAP therapy for 1 month. Plasma levels of NF-KB-controlled gene products were reduced in 4 out of 5 of these CPAP-treated subjects. These novel findings suggest that measuring NF-KB activity may be useful for assessing clinical impact of therapy with CPAP, just as measuring cholesterol fractions has become utilized to assess impact of drug therapy for hyperlipidemias. The routine measurement of NFKB is far from ready for prime time. This first report was small, and while A. H. Eliasson . C. J. Lettieri Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC 20307-5001, USA