Molecular mechanism studies have shown that activin A exacerbates myocardial metabolic disturbances by inhibiting INS-mediated phosphorylation in the PI3K/Akt signaling pathway, which is a key regulatory pathway for myocardial glucose uptake, revealing its central role in the pathological process of DCM (27). The gene discussed is AKT1; the disease is familial dilated cardiomyopathy.