Interestingly, recent evidence shows that perturbations in skeletal muscle sarcomere ultrastructure in individuals with heart failure and type 2 diabetes can be improved by stimulating mitochondrial function [49], which supports a close functional connection between mitochondrial alterations and muscle damage, and suggests that mitochondrial abnormalities observed in Stk25 transgenic muscle may have contributed to altered myofibril architecture. Here, STK25 is linked to type 2 diabetes mellitus.