This implies that such a heterozygous state of p53 is often transient during cancer progression and there is a selective force driving the inactivation of the remaining wild-type p53 allele in cancers, and also suggests that the dominant-negative effect of mutp53 is not sufficient to completely inactivate the remaining wild-type p53 allele in majority of cancers (Rivlin et al., 2011; Freed-Pastor and Prives, 2012). This evidence concerns the gene TP53 and cancer.