Retinoic acid (RA) is essential for many developmental processes, but signalling levels must be tightly regulated since too much RA signalling can cause developmental defects. Cyp26 enzymes help to control this balance, metabolising RA and ensuring the correct specification of multiple different organs. Loss of Cyp26 activity can affect heart formation, and now (see p. 1638) Ariel Rydeen and Joshua Waxman reveal a mechanism that may underpin this. The authors show that Cyp26 activity in the zebrafish anterior lateral plate mesoderm (ALPM) is required for the correct specification of cardiac versus vascular lineages. Specifically, loss of Cyp26 activity in zebrafish embryos results in an accumulation of RA and a subsequent increase in the specification of atrial cells at the expense of endothelial progenitors. The authors propose that the Cyp26 enzymes can have non-cell-autonomous consequences through regulating the amount of RA in the local environment to promote vascular specification by defining the boundary between atrial and endothelial progenitor fields in the ALPM.