Cardiomyocytes and myocardium from T2D mice show i) [Ca2+]d overload; ii) Reduced glucose uptake; iii) Elevated ROS generation; iv) Higher myocardial levels of TNF-α and IL-6 and expression of NF-κB; v) Increased calpain activity, cell injury, and reduced cell viability; vi) Reduced protein expression of KATP channel Kir6.2, SUR1, and SUR2 subunits. This evidence concerns the gene NFKB1 and type 2 diabetes mellitus.