Our analysis of genome-wide chromatin occupancy by p53 using ChIP-seq revealed the “p53 default program” (i.e., a similar pattern of p53 binding to chromatin in MCF7 breast cancer cells), irrespective of the activating compound (nutlin3a, RITA or 5-FU) and regardless of distinct transcriptional and biological responses triggered by these compounds [39]. The gene discussed is TP53; the disease is breast carcinoma.