The epiblast of mammalian embryos undergoes a period of rapid growth shortly after implantation, thereby establishing a population of cells that will give rise to the embryo proper. Here, Miguel Ramalho-Santos and co-workers show that chromodomain helicase DNA-binding protein 1 (Chd1) is required for the transcriptional output that drives this rapid growth (p. 118). They first show that Chd1–/– mouse embryos display post-implantation defects; analyses of lineage and patterning markers indicate that Chd1–/–embryos arrest in the transition between E5.5 and E6.5, prior to anterior-posterior patterning and the onset of gastrulation. The researchers further show that transcriptional output per cell is reduced in Chd1–/– mouse embryonic stem cells (ESCs) compared with control ESCs. In line with this, the amount of RNA polymerase II present at gene bodies and transcriptional start sites is decreased in mutant ESCs. Finally, the authors document that Chd1 also directly regulates the output of ribosomal RNA in both ESCs and the epiblast. In summary, the authors propose that Chd1 promotes a global increase in transcriptional output by both RNA polymerase I and II that, in turn, sustains the rapid growth of the epiblast.