Thus, hind-limb unloading, a model of disuse atrophy, resulted in a 10-fold increase in the activity of a transfected NF-κB-dependent reporter (Hunter et al, 2002), but this involved p50, c-Rel and Bcl-3 and not activation of p65 or I-κB, and is thus distinct from cachexia. The gene discussed is BCL3; the disease is Cachexia.