The results showed that the myocyte cross-sectional area was increased in the hearts of DCM mice, with elevated mRNA levels of ANP, BNP and β-MHC, while STING knockdown alleviated these phenomena, indicating STING deficiency dramatically inhibited the deterioration of cardiac hypertrophy in DCM mice (Fig. 2e–h). The gene discussed is STING1; the disease is familial dilated cardiomyopathy.