Striking molecular and developmental similarities in heart development exist between flies and vertebrates. For example, both develop from bilaterally symmetrical rows of mesodermal cells that fuse to form a heart tube, which in flies consists of outer pericardial and inner myocardial(cardioblast) cells. The factors that regulate heart development are also conserved between flies and vertebrates, including tinman (vertebrate NKX2.5), dpp (BMP2/4) and pannier (pnr, GATA transcription factor homologue). Now three Development papers shed new light on heart cell lineages and on the transcriptional mechanisms that control Drosophila heart development – findings that will inform studies of vertebrate cardiogenesis. When Alvarez et al. investigated the cardiogenic function of pnr and pointed (pnt),they found that they act sequentially: pnr acts early in mesoderm development to bring about cardiac mesoderm (CM) formation, and pntregulates CM cell fate choice. In its absence, cardioblasts form at the expense of pericardial cells, but only in the posterior domain of the heart. Importantly, their findings on p. 3015 indicate that a developmental and genetic distinction exists between the anterior and posterior regions of the heart, with potential functional consequences. Klinedinst and Bodmer, on p. 3027, also investigated pnr function and that of its binding partner u-shaped(ush) in loss-of-function and germ-layer-specific rescue experiments. They report that pnr and ush are required to initiate and maintain cardiogenesis, respectively, and for myocardial and pericardial cell fates to form. Pnr is also required in the ectoderm, where it might mediate and maintain cardiogenic dpp signalling. In a different approach, Han and Bodmer explored heart cell lineages by arresting cardiac cell divisions at various developmental stages. They found, on p. 3039, that the non-dividing progenitors of symmetric cell lineages adopt myocardial- or pericardial-only fates, whereas those of asymmetric divisions adopt a myocardial fate through the inhibition of Notch signalling.