Building on established roles of S100A9 in NF‐κB/p38‐mediated inflammation [27], rp‐S100A9 stimulation in HFL1 cells upregulated CCL‐2, IL‐6, and IL‐8 while suppressing ELN expression (Figure S10A), recapitulating COPD‐associated signatures [28, 29]. The gene discussed is S100A9; the disease is chronic obstructive pulmonary disease.