Genetic studies in GEMMs with reversible inactivation of p53 have shown that restoration of p53 leads to rapid regression of established tumors (Martins et al, 2006; Ventura et al, 2007; Xue et al, 2007), providing strong rationale for designing anti‐cancer drugs that restore p53 function by inhibiting MDM2 (Vassilev et al, 2004) or by restoring wild‐type function to mutant p53 (Bykov et al, 2002). The gene discussed is TP53; the disease is cancer.