IFNG and neoplasm: Modification of N-linked glycosylation of HCV E1 protein, a naturally poor immunogen, through site-directed mutagenesis of N-linked glycosylation sites in plasmids containing the genes for both wild type and mutant E1 in BALB/C mice resulted in enhanced E1-specific CTL activities, expression of IFN-γ producing T cells, and suppression of tumor growth E1-M2 mutant (at site of N209SS).