As with most novel research, the study by Colish et al9 has generated several questions for clinicians and scientists in the field. For the clinician, is CMR a useful clinical tool to monitor cardiovascular improvements, and will this approach help to improve CPAP adherence? Can pretreatment CMR act as a reliable marker for identifying patients at high cardiovascular risk, even possibly those with mild OSA, such that they can be rapidly provided with CPAP and comprehensive pharmacotherapy alongside intensive support to optimize adherence? Does the high cost of CMR outweigh these benefits in an era of health-care reform? For the scientist, what are the early pathologic and physiologic changes in the heart due to OSA, and what is the chronologic sequence and reversibility of these changes? Are there other surrogate cardiac imaging markers that could be used to detect adverse ventricular remodeling, even when chamber volumes, mass, and function appear normal? What duration of CPAP and level of adherence are required to see important changes in CMR? Can other OSA treatments, such as oral appliances, surgery, or alternative pressure modes, cause improvements in cardiac morphology and physiology similar to those seen with CPAP? Finally, if future studies are able to attribute irrefutably improvements seen with CMR to CPAP, are these changes predictive of hard cardiovascular end points such as myocardial infarction and stroke in OSA?