Mutation of all four residues blocked GATA4 acetylation and blunted cardiac hypertrophy induced by GATA4 overexpression, thus demonstrating the importance of GATA4 acetylation in the regulation of GATA4 transcriptional activity.55, 56 A recent study identified K311 (corresponding to K313 in the paper) as a primary target of acetyltransferases p300/CREP, with an enhanced cellular stability of acetylated GATA4.57 The study was carefully conducted to simulate the effect of loss‐of‐function by using lysine to arginine mutations for the optimal structural integrity of the mutated proteins. Here, GATA4 is linked to cardiac hypertrophy.