Three of the most common forms of human congenital heart defects result from aberrant asymmetric cardiac morphogenesis. Using zebrafish as a model, we aim to better understand the links between cellular aberrations during heart morphogenesis and the resulting cardiac defects. To that end, we have investigated the role of Fibroblast Growth Factor (FGF) signaling, which is known to couple morphogenesis to cell migration events in zebrafish, in asymmetric heart development. We have uncovered a role for FGF signaling in dextral looping that is independent of its early role in establishing left-right asymmetry. We find that treatment of embryos with the FGFR inhibitor SU5402 during different time windows results in defective cardiac looping and ballooning. Treatment from 24-30hpf affects both the position of the heart chambers as well as their morphology; however, treatment from 30-36hpf affects chamber morphology without significantly impacting chamber positioning. We thus propose that FGF signaling plays two different roles during late cardiac development: the promotion of dextral looping and of chamber expansion. We will present data that define the role of the pathway during event. .