As expected, introduction of just a single mutant p53 cDNA gene led to high steady-state levels of p53 that remained unchanged by treatment with nutlin-3A (Fig. 2b: lanes 9,10), and no functional responses of the p53 system (Fig. 2b,c) – a situation mimicking that encountered in many MM cell lines which display a TP53−/mut phenotype20. The gene discussed is TP53; the disease is Miyoshi myopathy.