In sepsis, CoA participates in the regulation of hepatic metabolism by modulating the expression of bile acid synthesis-related enzymes such as bile acid-CoA-amino acid N-acyltransferase (rBAT), with dysregulation potentially contributing to liver dysfunction and cholestasis—findings that reflect CoA’s complex role in coordinating inflammatory and metabolic stress responses [56]. The gene discussed is SLC3A1; the disease is Sepsis.