Several studies have shown that uric acid and ATP released from BLM‐injured lung cells constitute major endogenous danger signals that increase the mitochondrial reactive oxygen species (ROS) generation, and then activate the NALP3 inflammasome characterized by the maturation of pro‐caspase‐1, leading to IL‐1β production and pulmonary fibrosis 11, 12, 13, 14, 15, 16. The gene discussed is IL1B; the disease is pulmonary fibrosis.