Regulation of mRNA processing is a critical nodal point for dynamically altering gene expression during stress. From their biogenesis at the site of transcription, mRNAs associate with RNA-binding proteins that regulate their translation. How this process is functioning in the heart and contributes to disease states is still little understood. We discovered how chemical modifications on mRNA regulate heart stress responses. For this, we generated cardiac specific gain- and loss-of-function mouse model for METTL3 (Methyltransferase like 3); an RNA-modifying protein that deposits methylation marks on N6 position of adenosines (m6A). Our work defined the role of m6A in cardiomyocytes and the critical important of this modification for preservation of cardiac homeostasis and cell size regulation. Overall, our research has shed light on the pathophysiological relevance of post-transcriptional events for gene expression regulation in the heart.