s / Placenta 34 (2013) A1–A99 A6 majority of FGR cases remain idiopathic. These idiopathic FGR pregnancies are frequently associatedwith placental insufficiency, possibly as a result of placental maldevelopment. Understanding the molecular mechanisms of abnormal placental development in idiopathic FGR is therefore of increasing importance. The focus of our studywas to understand the role of homeobox gene transcription factors in abnormal placental development associatedwith human idiopathic FGR. The strategy we have employed has resulted in the identification of homeobox genes, which are expressed in normal placental development and that showed altered expression in FGR. Functional assays following target gene inactivation or over-expression to mimic FGR in cultured cells demonstrated that homeobox genes control important functions inplacental cells. The discoveryof targets of homeobox genes has revealed genes, and pathways, not previously implicated in FGR. These target genes and pathways will be further assessed for their therapeutic anddiagnostic potential for clinicalmanagementof idiopathic FGR in future. http://dx.doi.org/10.1016/j.placenta.2013.06.022 PL5.4. OMICS EXPLORATION OF PLACENTAL PATHOLOGIES AND DEVELOPMENT: TISSUES, CELLS AND GENES