Since IκBα has been suggested to be degraded in the proteasome and DSF has been shown to possess proteasome inhibition potential, we speculate that the general blockade of DSF on NF-κB transactivation is through proteasome inhibition [40–42].The corresponding decrease in OC formation and reduction in NF-κB signaling is consistent with the notion that NF-κB activation is vital to osteoclastogenesis which is best exemplified in studies of p50/p52 double knockout of NF-κB machinery in mice which exhibit greatly suppressed OC formation and osteopetrosis [43]. This evidence concerns the gene NFKB1 and osteopetrosis.