To investigate the role of Piezo1 in ILC2-mediated allergic inflammation and fibrosis, we utilized two physiologically relevant mouse models that are known to increase mechanical stress within the lung microenvironment: an acute IL-33-induced acute allergic airway inflammation model37,38 and a chronic bleomycin (BLM)-induced lung fibrosis model (Fig. 5a, g).39,40 In the IL-33 model, intratracheal administration of IL-33 induces rapid activation and expansion of ILC2s, leading to eosinophilic inflammation and mucus hypersecretion. The gene discussed is PIEZO1; the disease is inflammation.