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. Here, RIPK1 is linked to Sepsis.