The major findings of this study can be summarized as follows: (1) systemic and intrarenal proinflammatory cytokines were upregulated together with decreased renal CXCL14 expression in mice; (2) renal CXCL14 expression was negatively associated with the production of cytokines and the severity of AKI in septic mice; (3) overexpression of CXCL14 attenuated sepsis-associated AKI together with improved survival outcome; and (4) CXCL14 overexpression decreased M1 polarization but increased M2 polarization both in vivo and in vitro. Here, CXCL14 is linked to Sepsis.