Genomic imprinting marks a subset of mammalian genes for parent-of-origin-dependent monoallelic expression. Embryological and classical genetic experiments in mice that uncovered the existence of imprinting nearly two decades ago produced abnormalities of growth or behavior, without severe developmental malformations. Since then, the identification and manipulation of individual imprinted genes have continued to suggest that the diverse products of these genes are largely devoted to controlling pre- and postnatal growth, as well as brain function and behavior. We will review this evidence and discuss recent data from our lab pertaining to the imprinted gene Ipl/Tssc3. This gene lies in an extended imprinted region of distal mouse Chr7 that also contains the insulin-like growth factor 2 (Igf2) gene. Expression of Ipl is highest in placenta and yolk sac, where its mRNA is derived almost entirely from the maternal allele. Ipl encodes a small cytoplasmic protein with a pleckstrin-homology domain, a motif that binds to phospho-inositol lipids. To assess function in vivo, we constructed two lines of mice with germline deletions of this gene (IplNeo and IplloxP) and another line deleted for the similar but non-imprinted gene Tihl. All three lines are viable. There is consistent overgrowth of the Ipl-null placentas, with expansion of the spongiotrophoblast. However, these larger placentas do not confer a fetal growth advantage: fetal size is normal in Ipl-nulls with the IplNeo allele, and is slightly decreased in nulls with the IplloxP allele. When bred into an Igf2-mutant background, the Ipl deletion partially rescued the placental, but not fetal, growth deficiency. Neither fetal nor placental growth is affected by deletion of Tihl. These results show a non-redundant function for Ipl in restraining placental growth. The data further indicate that Ipl can act, at least in part, independently of IGF2 signaling. Thus, genomic imprinting regulates multiple pathways to control placental size. Maternal drive to restrain the size of this "parasitic" organ may be a sufficient evolutionary rationale for the conservation of imprinting at some loci.