To model the recessive, presumed loss-of-function TAF1A mutations, stable knockout of the single taf1a zebrafish homolog was performed, resulting in a frameshift mutation leading to a premature stop codon (Supplementary Material, Fig. S2). Homozygous mutant zebrafish embryos recapitulated a heart failure phenotype beginning at 6 days post-fertilization, with progressive pericardial edema and a significant decrease in ventricular fractional shortening compared to WT embryos (Fig. 3A and B). Knockout of taf1a resulted in early lethality, with embryonic death occurring 6 to 11 days post-fertilization (Fig. 3C).