Previous studies have shown that chronic inflammation driven by IL6 and macrophage-derived IL1β is associated with impaired alveolar regeneration through induction of damage-associated transient progenitors (DATPs) from AT2 cells that are unable to make a full transition to AT1 cells during pulmonary fibrosis in both humans and mice [18, 19]. The gene discussed is IL1B; the disease is pulmonary fibrosis.