During Drosophila heart development, intercellular signalling pathways activate a conserved cardiac-specific gene regulatory network by inducing the expression of the transcription factor Tinman (Tin) in the dorsal mesoderm. Stat92E, the transcriptional effector of the JAK/Stat signalling pathway, is a direct target of Tin and, on p. 4627, Eric Olson and colleagues characterise JAK/Stat signalling during cardiogenesis for the first time. They show that Drosophila embryos with mutations in the JAK/Stat ligand upd or in Stat92E have non-functional hearts with luminal defects and inappropriate cell aggregations. The JAK/Stat pathway, they report, is active in the dorsal mesoderm when the initially broad mesodermal expression pattern of tin becomes restricted to cardiac and visceral muscle progenitors, which occurs after dorsal mesoderm progenitor specification. Finally, they show that JAK/Stat signals activate Enhancer of Split complex genes to restrict Tin expression, thereby regulating heart precursor diversification. Overall, these findings show that JAK/Stat signalling regulates heart development and identify an autoregulatory circuit by which tin restricts its own expression domain.