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The rationale for subphenotyping acute respiratory distress syndrome (ARDS) arises from its marked biological and clinical heterogeneity. Crucially, the aim of subphenotyping is not merely classification, but the identification of underlying biological mechanisms that can inform targeted interventions. Subphenotypes are intended to capture ‘treatable traits’, highlighting patient groups that may respond differently to specific therapies. When these traits are truly rooted in pathobiology, they should be consistent across geographical regions and clinical contexts.1 Conversely, if they are shaped by local factors or variations in supportive care, their applicability may be limited. This tension underscores the need to distinguish fundamental biological features from context-specific influences within ARDS subphenotyping.2