Treatment with the proteasome inhibitors lactacystin (LAC) or MG132, substantially extended the half-life of endogenous Ajuba in BEL7402 and HepG2 cells (Fig. 5a, right panels showing statistical analyses of the quantification of Ajuba protein level), suggesting that the degradation of Ajuba in HCC cells is proteasome-dependent. The gene discussed is AJUBA; the disease is hepatocellular carcinoma.