Besides, metabolic status and monocyte trafficking could also influence adaptive immunity to bacterial infection.[56, 70] Given that hepatocytes are the principal cells in the liver and we did not see altered bacterial loads in WT and Alb‐Cre TMEM16F KO mice, we believe that the changes in lipids observed in our liver lipidome results are likely due to dysregulated metabolism indirectly elicited by excessive inflammation triggered by KCs death. Here, ALB is linked to bacterial infectious disease.