First, the reliance on murine models (CLP and LPS) restricts direct translation to human sepsis, which exhibits greater etiological and immunological heterogeneity.[61, 62, 63, 64] While plasma P‐RIPK1 levels correlated with disease severity in sepsis patients, direct evidence of the JAK1‐STAT3‐CXCL1 axis in human lungs remains to be established. This evidence concerns the gene CXCL1 and Sepsis.