Fetal growth restriction (FGR) is a major threat to human health impacting neonatal survival and increasing the risk of behavioural and metabolic disorders later in life, a phenomenon described as fetal programming or developmental origins of disease. Higher than normal placental expression of the imprinted gene PHLDA2 has been reported in a number of studies of FGR, fetal death and low birth weight. We modelled this specific alteration and demonstrated that two-fold increased expression of Phlda2 is sufficient to reduce birth weight by 10% followed by rapid postnatal catch-up (1). We further showed that Phlda2 functions to negatively regulate the endocrine compartment of the placenta (2) and, through this function, influences the behaviour of wild type mothers towards their offspring (3). Being born small and being exposed to suboptimal maternal care are both risk factors for behavioural disorders in human populations. We therefore undertook a behavioural and molecular characterisation of Phlda2 transgenic and non-transgenic littermates alongside concurrently bred fully wild type cohort. Offspring exhibited increased anxiety-like behaviours, deficits in cognition and atypical social behaviours alongside changes in the transcriptional signatures of key brain regions with males relatively more impacted than female (4). Our work establishes, for the first time, the experimental paradigm that placental endocrine insufficiency programs atypical behaviour in both mothers and their offspring. Importantly, we have evidence that this mechanism may contribute to the co-occurrence of low birth weight and perinatal mood disorders in human populations.