Although the molecular mechanisms underlying this process are not well established yet, the increase of intracellular NO levels within the cell seems to be capable of mediating FoxO3a activation and nuclear translocation, thereby inducing skeletal muscle atrophy by upregulating MuRF1 or atrogin-1/MAFbx [79, 80]. This evidence concerns the gene FBXO32 and Skeletal muscle atrophy.