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is entirely justifiable, as it represents powerful, data-driven medicine. Would the identification of particular metabolites or their fragments by GC-MS in exhaled air by itself qualify for unraveling the critical pathobiological pathways in relation to eosinophilic or neutrophilic inflammation? This is unlikely, as the “big brothers” of this technology, such as transcriptomics and proteomics, are much closer to the mechanistic networks and are delivering at present (3, 4). The prospect of using GC-MS in this context is therefore twofold. First, when associating the present VOCs with accompanying RNA and protein profiles, it might become feasible to indirectly establish any transcriptomic or proteomic fingerprints of asthma by noninvasive analysis of exhaled VOCs. Then breathomics is used for rapidly recognizing elaborate biological phenotypes, as has been done by Brinkman and colleagues for electronic nose (eNose) profiles against sputum transcriptomics profiles (8) (data in online supplement). Second, GC-MS data from the present study can also be used for tailoring crossreactive sensors for eNoses toward their most discriminative and evidence-based combination for establishing eosinophilic or neutrophilic inflammation (9). Notably, eNoses have also been trained and validated in discriminating eosinophilic and neutrophilic inflammation with high accuracy, regardless of the clinical diagnosis of asthma or chronic obstructive pulmonary disease (8, 10). The advantage of the latter technology is that it can be linked to big online databases and cloud computing, providing real-time results in the doctor’s office (www.breathbase.org). The article by Schleich and colleagues (7) presents a landmark study on the validation of exhaled VOCs in the inflammatory profiling of asthma. This is needed for type 2 and increasingly also for non–type 2 asthma phenotypes. Ongoing clinical tailoring of breathomics is definitely bringing data-driven, precision medicine to the point of care.n

Seeing the Forest for the (Arterial) Tree: Vascular Pruning and the Chronic Obstructive Pulmonary Disease Pulmonary Vascular Phenotype