These studies revealed recurrent alterations in tumours, including the loss of the tumour suppressor gene phosphatase and tensin-homolog (PTEN), gains of the genes encoding transcription factors androgen receptor (AR) and proto-oncogene c-Myc (MYC), recurrent mutations of genes encoding the cell cycle regulator retinoblastoma associated protein (RB), E3 ubiquitin ligase adaptor Speckle Type BTB/POZ Protein (SPOP), tumor suppressor p53 (TP53), and fusion of E26 transformation-specific family (ETS-family) transcription factor genes with androgen-responsive promoters [12,14,15,20,21,22]. The gene discussed is TP53; the disease is neoplasm.