We showed here that the phosphorylated p38 (p-p38) level was significantly increased in the myocardium of TAC mice and in Ang II-stimulated H9C2 cardiomyocytes, while SYT1 KO or silencing exacerbated these effects, suggesting that SYT1 can adversely regulate cardiac hypertrophy mainly via affecting the phosphorylation of p38. The gene discussed is AGT; the disease is cardiac hypertrophy.