Using genetic and pharmacological approaches in murine models, we aim to delineate the spatiotemporal activation of RIPK1 in AECs during sepsis, elucidate its mechanistic link to JAK1‐STAT3‐mediated CXCL1 transcription, and evaluate the efficacy of a novel RIPK1 inhibitor, compound 62,[29] in mitigating lung injury. Here, CXCL1 is linked to Sepsis.