Defects in placental growth and patterning can have severe consequences for foetal health, and can cause intrauterine growth restriction (IUGR). However, relatively little is understood about the mechanisms regulating placental development, particularly the later phase of maturation when the blood vessels of the so-called labyrinth elongate and elaborate. On p. 1976, Paul Delgado-Olguin and colleagues show that the histone methyltransferase G9a is required for placental maturation. Endothelial-specific knockout of G9a in mice has no effect on early placental development, but mutants show severe defects in labyrinth size and structure after mid-gestation, owing to reduced proliferation of endothelial cells. Intriguingly, the authors provide evidence for non-autonomous regulation of trophoblast cell proliferation, which is upregulated in the endothelial-specific knockout. G9a conditional mutants show reduced expression of Notch pathway effectors (previously implicated in regulation of placental maturation), and the placental vessel phenotype can be rescued by activation of the Notch pathway. Thus, G9a is a key regulator of placental maturation in mice, regulating the balance of endothelial versus trophoblast proliferation. Notably, this mechanism may also apply in human, since G9a and Notch pathway components show altered expression in samples from IUGR pregnancies.