Recently, we found that knockdown of the BH3-only molecule Bad correlated with the upregulation of both apoptotic and oxidative stress genes. Furthermore, this Bad knockdown-mediated environmental stress can further influence normal cell migration in the formation of the three germ layers, especially the ectoderm, for further brain development, but very few studies have addressed Bad function in the molecular mechanisms of brain embryonic development. In a zebrafish system, we identified a new role for the BH3-only domain Bad in triggering PCD during early embryonic development, related to completion of the development of tissues or organs, such as the brain, by affecting some novel gene expressions during early development. These functions and the relationship between p53-mediated stress signaling on the caspase-8/tBid cell death pathway and brain-development-related regulation should all be further addressed.