Furthermore, ALKBH5 overexpression has also been shown beneficial by enhancing cardiac regeneration and salvage myocardial function after MI in both neonatal and adult mice (see section “cardiogenesis and cardiac regeneration”) via m6A demethylation-dependent increase in Ythdf1 translation and consequent YTHDF1-dependently enhanced Yap1 translation to YAP1.54 Here, YTHDF1 is linked to myocardial infarction.