Although it remains to be studied if NGFR can also regulate p53 stability and activity in a negative feedback fashion in normal nerve systems, our findings demonstrate that cancer cells hijack this anti-p53 activity of NGFR toward their growth advantage in a way similar to that for MDM2 and MDMX inactivation of p53 in cancers (Momand et al., 1992; Oliner et al., 1992, 1993; Shvarts et al., 1996; Wu et al., 1993), as knockdown of NGFR markedly induced p53-dependent apoptosis and cytotoxicity as well as eliminated xenograft tumor growth (Figures 2–8). The gene discussed is TP53; the disease is neoplasm.