These protein-level findings corroborate our mRNA expression data, demonstrating that: (1) ALF induces coordinated upregulation of UII and downregulation of Ces1f; (2) Urantide effectively normalizes these pathological alterations; and (3) The UII/UT signal blocker specifically modulates Ces1f expression during inflammatory injury without influencing physiological homeostasis, highlighting its potential as a therapeutic target for acute liver failure. This evidence concerns the gene UTS2 and acute liver failure.