JAK1 and Sepsis: Sepsis‐induced lung injury, characterized by dysregulated inflammation and alveolar epithelial damage, poses a significant clinical challenge.[2, 3] This study reveals a novel mechanism by which receptor‐interacting serine/threonine‐protein kinase 1 (RIPK1) drives neutrophil‐mediated lung injury through the JAK1‐STAT3‐CXCL1 signaling axis in alveolar epithelial cells (AECs), highlighting RIPK1's functionality beyond necroptosis and redefining alveolar structural cells as active contributors to inflammatory amplification.