Taken together, these data support a two-limb model: (i) very low BHB in cirrhosis may reflect severe mitochondrial failure because of functional and architectural damage; (ii) very high BHB—whether in cirrhosis or in the general population—marks a catabolic-stress phenotype characterized by unopposed lipolysis, insulin resistance, and systemic inflammation. The gene discussed is INS; the disease is Cirrhosis.