In the presence of a second oncogenic hit or loss of a tumor suppressor such as Tp53, tumor progression is accelerated, with accompanying genetic instability reflected in copy number variations and aneuploidy (Ruggeri et al. 1991; Kemp et al. 1993; Lazarov et al. 2002; Dajee et al. 2003; Chen et al. 2009; Lapouge et al. 2011; White et al. 2011; Nassar et al. 2015). The gene discussed is TP53; the disease is neoplasm.