Nearly 1% of newborn babies have heart defects, often caused by abnormal cardiac outflow tract (OFT) development. The OFT is initially a myocardial tube that forms from a mesodermal cell population called the second heart field (SHF). During OFT remodelling, the myocardial cells secrete extracellular matrix (ECM) to form the OFT cushions, which are invaded by neural crest cells and by endothelial cells that line the OFT myocardium. The endothelial cells undergo an endothelial-to-mesenchymal transition (EMT) and,finally, the OFT septates into the aorta and the pulmonary artery and realigns/rotates into its final position. Two papers in this issue of Development provide new information about how FGF signalling controls these complex morphogenetic events in mice. On p. 3599, Anne Moon and colleagues report that an FGF signal produced in the SHF mesoderm establishes an autocrine loop that regulates OFT development in vivo. The researchers inactivate two FGF receptors (Fgfr1 and Fgfr2)and overexpress the FGF antagonist sprouty 2 in various embryonic cell types to dissect FGF's role during OFT development. Unexpectedly, given the paradigm of FGF paracrine signalling established in other tissues, the neural crest cells and endothelial cells are not the direct targets of the SHF-derived FGF. Instead, interrupting FGF signalling in SHF mesodermal cells prevents the secretion of signalling and ECM factors by their progeny, which secondarily perturbs endothelial and neural crest cell invasion into the OFT cushions, and also the EMT and OFT septation. On p. 3611, Fen Wang and colleagues use ablation of Frs2α, which encodes an adaptor protein that links FGF receptor kinases to multiple signalling pathways, to investigate the downstream pathways that mediate FGF signalling in cardiac progenitors. They report that ablation of Frs2α in SHF mesodermal cells affects their expansion into the OFT myocardium and results in OFT misalignment and hypoplasia. In addition, EMT and neural crest recruitment into the OFT cushions are defective in Frs2αmutants, resulting in OFT septation defects. Taken together, the results of these two papers provide new molecular insights into the regulation of OFT morphogenesis by FGF signalling.