Each p53 tetramer presents a dimer of dimers where the primary dimer is formed via hydrogen bonds and salt bridges, and the tetramer is generated by hydrophobic interactions.[12] Mutations in the tetramerization region (TET) can alter the oligomeric state of p53 and have so far been observed in various human cancers.[13] By substituting a single amino acid, interactions between p53 monomers can be disrupted, thereby affecting oligomer formation. The gene discussed is TP53; the disease is cancer.