Skeletal muscle mitochondria are appealing treatment targets, since mitochondrial dysfunction and high ROS generation have been reported by us and others in CHF models [14,16] and patients [11,43], and may lead to tissue oxidative stress, inflammation, and insulin resistance with strong muscle-catabolic potential [9,10,12,14,43,44], as indeed confirmed in this study. This evidence concerns the gene INS and congestive heart failure.