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Double mutant embryos carrying a deletion around the<jats:italic>H19<\/jats:italic>region and also a targeted<jats:italic>Igf2r<\/jats:italic>allele, both inherited maternally, have extremely high levels of IGF-II (7- and 11-fold higher than normal in tissues and serum, respectively) as a result of biallelic<jats:italic>Igf2<\/jats:italic>expression (imprint relaxation by deletion of<jats:italic>H19<\/jats:italic>-associated sequence) in combination with lack of the IGF2R-mediated IGF-II turnover. This excess of IGF-II causes somatic overgrowth, visceromegaly, placentomegaly, omphalocele, and cardiac and adrenal defects, which are also features of the Beckwith\u2013Wiedemann syndrome (BWS), a genetically complex human disorder associated with chromosomal abnormalities in the 11p15.5 region where the<jats:italic>IGF2<\/jats:italic>gene resides. 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