In STZ-induced T1D and STZ/high-fat diet-induced T2D murine models, GCN2 deficiency significantly attenuates DMCM pathological remodeling—including myocardial hypertrophy, fibrosis, and lipid deposition—concomitant with reduced myocardial p-eIF2α, GRP78, CHOP, ATF4, and Bax levels alongside elevated Bcl-2. This evidence concerns the gene BAX and type 2 diabetes mellitus.