During embryonic development, IGF-1 has two receptors. One will result in cell growth, while the other seems to bind to IGF-1 without effect. This false receptor is encoded by a gene that is indistinguishable from a sugar binding protein. When the IGF-1 gene is inherited from the father, it is active and produces growth hormone. When the IGF-1 gene is inherited from the mother, it is inactivated. Conversely, when the false receptor is inherited from the father, it is inactive, while the maternally-inherited gene is active.

So?

It can be considered that larger offspring serve the interests of the father, who wants his offspring to be stronger and better adapted to survive. On the other hand, the maternal agenda would be to have more moderately sized offspring that will not be so risky to carry and birth. So, paternally activated growth hormone is countered by maternally activated false growth hormone receptors.

This kind of gene regulation is called "genomic imprinting". It is a strategy used on a number of different genes for different apparent purposes. This particular example is sometimes seen as a 'battle of the sexes', but is illustrative of the forces that can shape the evolution of gene expression strategies.

See this article on the evolution of genomic imprinting at PubMed. PubMed is a repository of research articles at the National Library of Medicine, and access to many of these articles is free (your tax dollars at work).