While the increase in Sct serum levels (observed in patients with alcoholic cirrhosis) supports the concept that Sct triggers hepatobiliary damage and liver fibrosis, the increase in HCO3− levels in bile samples (although not significant) from patients with alcoholic cirrhosis may be due to a compensatory secretory repair mechanism by adjacent non-senescent cholangiocytes which may secrete HCO3− by Ca2+-dependent Cl− channels (e.g., transmembrane member 16A (TMEM16A) [49] independent of cAMP signaling, however, further studies are necessary to support this concept. This evidence concerns the gene ANO1 and Hepatic fibrosis.