Some of the possible theories for HCV induced lymphoma genesis include (a) continuous external stimulation of lymphocyte receptors by viral antigens and consecutive proliferation, (b) HCV replication in B cells with oncogenic effect mediated by intracellular viral proteins, (c) permanent B cell damage, for example, mutation of tumor suppressor genes, caused by a transiently intracellular virus (hit and run theory), and (d) prevention of B cell apoptosis by downregulation of caspase 1 and caspase 4 [13, 14]. Here, CASP4 is linked to neoplasm.