During vertebrate heart development, cardiac progenitors form bilateral fields within the lateral plate mesoderm that move towards the embryonic midline and fuse to form the heart tube. It is generally accepted that, during this process, in addition to its inductive signalling role, the endoderm serves as a mechanically passive substrate for the migrating cardiogenic mesoderm. Now, Victor Varner and Larry Taber suggest that the endoderm also has an active mechanical role during heart tube assembly (see p. 1680). Using label-tracking experiments in combination with actomyosin inhibitors, the researchers show that, in chick embryos, the endoderm actively shortens around the anterior intestinal portal, and that myosin-II-dependent contraction drives this shortening. Inhibition of contractility using actomyosin inhibitors, they report, produces cardia bifida and foregut defects. Moreover, computational modelling suggests that the endoderm (not the mesoderm) is the dominant contractile tissue layer during heart field migration. Thus, the researchers suggest, during avian cardiogenesis, active contraction of the endoderm pulls the heart fields towards the embryonic midline.