Taken together, the tumor-induced muscle atrophy is likely due to elevated levels of TNF-α and myostatin, which act together to activate NF-κB and FoxO1 so as to amplify the expressions of calpain (autolysis) and ubiquitin ligases (ubiquitin-proteasome) (Figure 5E). Here, NFKB1 is linked to neoplasm.