The preferential selection of missense mutants together with their excessive stabilization therefore points at additional mechanisms that promote tumor development beyond a mere loss of DNA binding activity: Missense mutants exhibit dominant‐negative effects on remaining wild‐type p53 and display neomorphic properties that—like an oncogene—actively drive tumor development to a metastatic and drug‐resistant state (Freed‐Pastor & Prives, 2012; Muller & Vousden, 2014; Kim & Lozano, 2018; Stiewe & Haran, 2018). This evidence concerns the gene TP53 and neoplasm.