METTL3 and heart failure: Increasing the expression of the m6A methyltransferase METTL3 in the heart drove spontaneous, compensated hypertrophy but did not affect cardiac function, whereas METTL3 knockdown led to morphological and functional signs of heart failure, which demonstrated that METTL3 may have the ability to block maladaptive eccentric remodelling [73] (Fig. 2b).