In a mouse model of multistage carcinogenesis elicited by the SV40 large T–antigen (Tag) oncogene in pancreatic β cells, the gene for insulin–like growth factor IGF2 is focally up–regulated and functionally implicated in tumour development. The IGF2 gene is differentially regulated in normal tissues: the paternal allele is transiently expressed during embryogenesis, whereas the maternal allele is genomically imprinted and inactive. Crossbred mice carrying the Tag oncogene and a disruption of either the paternal or maternal allele of IGF2 reveal that both alleles are co–activated early during tumour development, and that each contributes to malignant hyperproliferation and consequent tumour volume.