In the present study, we demonstrated upregulation of Sct/SR signaling in ALD evidenced by: (i) enhanced immunoreactivity/expression of Sct/SR/CFTR in an ALD mouse model and Sct/SR/CFTR/AE2 axis in liver sections from patients with alcoholic cirrhosis; and (ii) higher levels of Sct in serum from EtOH-fed WT mice as well as patients with alcoholic cirrhosis and higher bicarbonate levels in bile from patients with alcoholic cirrhosis compared to the respective controls. The gene discussed is SCT; the disease is alcoholic liver cirrhosis.