Interestingly, classic molecular markers of pathological cardiac hypertrophy such as nppa, nppb, myh7, and acta1a were not upregulated in mutant zebrafish hearts.34 However there was some overlap between transcriptional pathways in the vegfchy−/−;vegfd−/− mutant ventricles and the molecular programs associated with established experimental models of physiological and pathological cardiac hypertrophy in mice.35 In particular, pathways related to cell proliferation and lipid metabolism were enriched in mutant zebrafish hearts and mouse hearts subjected to pressure overload. Here, NPPB is linked to cardiac hypertrophy.