The gene encoding Fibroblast growth factor 10 (Fgf10) is expressed in cardiac progenitor cells of the second heart field (SHF). Situated in pharyngeal mesoderm in the early embryo, cells of the SHF contribute to the poles of the elongating embryonic heart and ultimately to the outflow tract, right ventricle and part of the atria. Mechanisms controlling SHF deployment are crucial for heart development and impairment of SHF addition leads to congenital heart defects including conotruncal and atrial septal defects. Fgf10 mutant embryos die at birth with severe defects in diverse developmental processes including failure of lung and limb formation, however, loss of Fgf10 does not have a major impact on SHF development and normal heart tube elongation and conotruncal septation is observed in Fgf10-/- embryos. Nevertheless, Fgf10-/- hearts present altered morphology with abnormal positioning of the apex in the thoracic cavity. Despite recent advances in our understanding of fetal heart growth, the molecular mechanisms controlling cardiac myocyte proliferation remained poorly defined. Here we show that Fgf10 is involved in the regulation of fetal cardiomyocyte proliferation. Fgf10 expression persists in the fetal heart prominently in the SHF-derived right ventricle. Analysis of Fgf10-/- fetal hearts reveals impaired proliferation of right ventricular myocytes associated with upregulation of the cell cycle inhibitor p27kip1, leading to altered right ventricular morphology. Our results reveal complex temporal and regional specific regulation of myocyte proliferation in the developing ventricles.