Under pressure overload, TASK-1 knockout mice have better cardiac function and reduced cardiac hypertrophy than normal mice, which may be related to the enhanced fatty acid oxidation by AKT phosphorylation and peroxisome proliferator-activated receptor-γ coactivator-1α, suggesting that TASK-1 may be involved in the pathophysiphysiological process of cardiac hypertrophy and heart failure (Duan et al., 2020). This evidence concerns the gene AKT1 and cardiac hypertrophy.