These results suggested that CCR9 could promote hypertrophy mainly due to the protein kinase B mammalian target of the rapamycin GSK-3β signaling cascade, rather than through the MAPK signaling pathway, which indicates that CCR9 can be used as a new regulator of myocardial hypertrophy and may provide a novel therapeutic target for suppressing myocardial hypertrophy in the future (Xu et al., 2016). This evidence concerns the gene AKT1 and cardiac hypertrophy.