Even though 35–50% of cancers do not have any TP53 mutation, it has been shown that various proteins can inhibit wild-type TP53 functions by accelerating its degradation [50,51,52,53,54,55,56,57] or blocking its oligomerization [51,58,59], such as Rab-like protein 1A (RBEL1A) [58]. The gene discussed is TP53; the disease is cancer.