There are several possible explanations, including increased passive transfer of dIgA across the blood-gut barrier with reduced oncotic pressure, reduced hepatic clearance from plasma, or increased production and secretion into the blood by enterocytes or hepatocytes in response to greater bacterial translocation across the gut wall in states of gut leakage.16,34 Our work does not answer this question and further studies are needed to elucidate the underlying mechanisms of dimeric IgA elevation in cirrhosis. This evidence concerns the gene CD79A and Cirrhosis.