To further decipher the molecular mechanism by which Paxillin- and FAK deficiency led to contractile dysfunction and heart failure in the zebrafish heart in vivo, we investigated the role of Vinculin in Paxillin/FAK-mediated heart failure, since it was recently shown that FAK and Paxillin are required to recruit Vinculin to Focal Adhesion (FA) sites, at least in mouse embryonic fibroblasts [22]. Here, VCL is linked to heart failure.