The role of HBV in the mechanism of DLBCL had not been fully elucidated; one hypothesis was that, like hepatitis C, a protracted antigenic stimulation of B cells produced virus-specific antibodies; another hypothesis was based on genome-wide analysis, which revealed that enhanced gene mutation load possibly mediated by apolipoprotein B mRNA-editing enzyme catalytic polypeptide (APOBEC) enzyme activity and the activity of the B-cell-specific activation induced cytidine deaminase (AID) (1, 15). This evidence concerns the gene APOB and hepatitis C virus infection.