These findings suggest that in Akt2‐KO or MT‐TG/Akt2‐KO mice increased Akt1 phosphorylation could compensate for other Akt2 functions but only minimally for glucose metabolic signalling to maintain glucose metabolism, therefore, resulting in typical T2D phenotype, as illustrated in Figure 8A, 11, 12, 13, 18; Thus, the protective effect of cardiac overexpression of MT in MT‐TG/Akt2‐KO mice cannot be attributed to MT's stimulation of Akt1 function to preserve the almost normal level of glucose metabolism‐associated pathways, as illustrated in Figure 8B. The gene discussed is AKT2; the disease is type 2 diabetes mellitus.