In the present study with Akt2‐KO mice, we also found that cardiac overexpression of MT was able to preserve almost normal levels of Akt2 downstream glucose transport and metabolism‐associated molecule expression and function, and prevent oxidative damage in MT‐TG/Akt2‐KO mice, therefore, the MT prevention of DCM in Akt2‐KO mice could not be mediated by its preservation of Akt2 expression and function through suppressing Trb3 as Akt2 negatively regulator, so alternative mechanisms must be implicated. The gene discussed is AKT2; the disease is familial dilated cardiomyopathy.