Reduced exogenous exposure of patients to VIT-D sources, intestinal malabsorption of dietary VIT-D3, reduced endogenous production of VIT-D binding protein and albumin, impaired hepatic hydroxylation of 1,25-OH-vitamin D3 to 25-OH-vitamin D3 and increased catabolic removal of 25-OH-vitamin D3 are described as responsible mechanisms for the VIT-D deficiency in cirrhosis [4]. This evidence concerns the gene ALB and Cirrhosis.