Structural homology between the DBD domains (Figure 2B) explains why p53 and p73 transactivate many of the same target genes, such as PUMA, CDKN1A, or BAX. Similarly to p53, p73 maintains the tumor suppressor function by guarding the genomic stability and driving cell cycle arrest, replicative senescence or apoptosis [78,79]. This evidence concerns the gene TP73 and neoplasm.