Genomic imprinting allows parent-of-origin specific control over gene expression. Although imprinted genes (or entire chromosomes) are homologous sequences that can be inherited from either parent, they are differentially marked by a heritable epigenetic modification (imprint), which can condition their behavior in term of gene expression. Imprinting-based regulation of entire chromosomes is observed in both insects (paternal genome elimination) and mammals (nonrandom X inactivation). Until recently, it was unknown whether plants possessed a similar epigenetic system discriminating between homologous chromosomes from either paternal or maternal origin. There is now experimental evidence for a genome-wide imprinting phenomenon during seed development in Arabidopsis. Genomic imprinting at the gene (or locus) level is observed in both mammals and flowering plants. In maize, only a few allelic variants of several nonessential genes expressed in the endosperm are imprinted. In Arabidopsis, gene-specific imprinting has recently been demonstrated for the MEDEA (and FIS2) gene, which is essential for normal seed development. Unlike the imprinted maize genes, so far all tested MEA alleles are subjected to regulation by imprinting. MEDEA and FIS 2 are members of the FIS class of genes (FERTILIZATION INDEPENDENT SEED) involved in regulation of growth and cell proliferation during seed development. MEDEA shares several paradigmatic features with imprinted mammalian genes. The MEDEA phenotypes provide empirical support for theories of an intragenomic parental conflict during seed development, whereby imprinting is proposed as a means to differentially balance the selfish interests of each sex's genome during the development of the progeny.