One of the most fascinating aspects in the formation of the heart is the very early development of the electrical patterning as can be registered by the ECG, which is the registration of the rhythmic waves of depolarizing activity over the cardiac muscle. In the mature heart the conduction system is held responsible for the rhythmic excitations and contractions. However, in chicken embryos of less than three days of development, when the formation of the atrial and ventricular working myocardium has just been initiated, an adult type of ECG can be monitored. Generally, the conduction system is defined as the system of specialized myocardial tissues responsible for initiation and propagation of the sinus impulse. If we accept this functional definition, then the early embryonic heart has a conduction system, which is already in place, because there is an adult type of ECG. On the other hand, if we would apply strict anatomical and histological definitions, the embryonic heart undeniably lacks a conduction system. This field of tension concerning the recognition of the conduction system using physiological versus anatomical or histological criteria has led to many controversies in the field of the development of the ‘cardiac specialized tissues’. Why certain areas of the heart tube do not develop into the working myocardium of the chambers and contribute to the formation of the cardiac conduction system is one of the key questions of cardiac embryology. By our recent findings that the transcriptional repressors Tbx2 and Tbx3 repress working myocardium formation, we are beginning to understand these morphogenetic processes. Detailed reconstructions of the developmental patterns of expression of Tbx3 during development have revealed that Tbx3 is expressed in those areas of the heart tube that do not become working myocardium, i.e. in the sinus node region, internodal region, atrioventricular junction, atrioventricular bundle and bundle branches. These areas comprise not only the conventional conduction system, but also the highly controversial areas of the internodal region and the entire atrioventricular junction. Cells are added continuously to the venous pole of the heart. An intriguing question is how the growing embryonic heart tube maintains the leading pacemaker at the inflow of the heart. Polarity along the longitudinal axis of the initial heart tube ensures that in the very early phases of heart development the dominant pacemaker is at the inflow of the heart. With the subsequent growth of the heart, so-called sinus venosus myocardium is added at the intake of the heart. The addition of this venous myocardium is under control of the T-box transcription factor Tbx18. Initially, this myocardium does not express the transcription factor Nkx2-5, which, in turn, permits the gene encoding pacemaker channel Hnc4 and Tbx3 to be expressed here. Upon maturation, the venous myocardium acquires the atrial phenotype, except the sinoatrial region where Tbx3 controls the maintenance of the nodal phenotype. Thus, the most recently added myocardium always has the highest pacemaker activity, which is lost upon maturation of the myocardium toward the atrial lineage. The sinus node escapes this maturation by the action of Tbx3. Finally, an ever recurring theme is whether the embryonic origin of the pulmonary myocardium would explain the frequent occurrence of arrhythmias taking origin from this region. Some groups suggest a common origin of the systemic myocardium, which includes the sinus node, and pulmonary myocardium. This would explain that arrhythmias can originate from other regions such as the pulmonary vein myocardium. It is common wisdom that fish do not have lungs, and only systemic venous returns where pacemaker activity resides. During evolution the pulmonary venous return developed at the dorsal side of the atrium in the pulmo-pharyngeal region. It is fascinating to observe that all recent molecular data have demonstrated that the pulmonary myocardial lineage is essentially different from the systemic myocardial lineage. These data have fundamentally changed our interpretations of these arrhythmias.