Though our dataset lacked the specific plasma proteins needed to directly apply subphenotyping schema published by other groups (e.g., IL-8, protein-C), the separation of clinical variables and plasma cytokines was similar to a pneumonia subphenotyping study in Europe,11 and to ARDS “hyperinflammatory” and “hypoinflammatory” subphenotypes.5 The gene discussed is CXCL8; the disease is pneumonia.