Although the mouse p15smArf protein lacks amino acid residues required for interacting with Mdm2 and is overtly deficient in triggering p53-dependent tumor suppressor activity, it surprisingly rescues focal developmental defects observed in Arf-null mice that synthesize neither p19Arf nor p15smArf; conversely, mice engineered to produce only a mutant p19Arf-M45A protein (encoding alanine in lieu of M45) retain p53-dependent tumor suppressor activity but continue to exhibit the fully penetrant developmental ocular and spermatogenesis defects seen in Arf-null animals [2]. The gene discussed is TP53; the disease is neoplasm.