Importantly, overexpression of YTHDF2 or METTL3 in BHPF-treated zebrafish embryos could partially rescue both ferroptosis-mediated heart failure (Fig. 4E, F) and apoptosis-mediated CVP defects (Fig. 4G, H), indicating m6A/YTHDF2-mediated regulation played a critical role in modulation of these two mechanistically independent and tissue-specific ferroptosis and apoptosis processes upon BHPF exposure in the same organism (Fig. 4I). Here, METTL3 is linked to heart failure.