Classical and alternative NF-κB signaling pathways have been shown to have divergent roles in muscle in response to cytokine mediated atrophy and during muscle development [18], [35], [36], [37], however since we found evidence for IKKβ, and not alternative NF-κB signaling in C26 cachexia, those divergent actions do not appear to function here. This evidence concerns the gene IKBKB and Cachexia.