First, because of the anatomical constraints of the thoracic cage, TUS at its best explores about 70% of the pleural surface. Even in amenable zones, TUS visualizes only the lesions adherent to the pleural surface. Moreover, TUS may provide similar patterns in many diseases reducing lung aeration in the subpleural surface and does not distinguish among different causes of consolidation, for instance between pneumonia and atelectasis, which may coexist. In addition, even children with normal lungs often display subsegmental lung focal areas of atelectasis beyond terminal bronchioles (Fig 1). The picture is further compounded by artifacts, predominantly B lines. The latter are generated behind the pleural line by the elevated difference of acoustic impedance between either soft tissue or fluid and gas. B lines may be detected in several pleuropulmonary diseases; their number has low specificity and does not allow discrimination between different conditions. In summary, no feature of TUS can be considered at all disease specific. In addition, the authors particularly emphasized the results concerning “linear/arborescent bronchograms.” However, to our knowledge, no study or meta-analysis hitherto has demonstrated that they really match the anatomy of the bronchial tree or the CT finding of an air bronchogram, this TUS sign being detectable even in lung neoplasms. The authors also stressed the sign of the “double lung point,” which is a TUS sign of pneumothorax. The same term has been used previously to describe a TUS sign of transient tachypnea of the newborn subsequently renamed “double transition point.” Finally, the authors did not provide information on several settings parameters (time gain compensation, tissue harmonics, and electronic focus), which may affect the ultrasonographic pattern.