In vitro and cell-based analyses have shown that tumor-associated hotspot mutants of p53 lack intrinsic DNA binding and fail to occupy wild type p53 binding sites that conform to the well characterized consensus (Bargonetti et al, 1991; Bargonetti et al, 1993; Cho et al, 1994; el-Deiry et al, 1992; Joerger et al, 2006; Joerger et al, 2005; Kato et al, 2003; Kennedy and Lowe, 2022; Kern et al, 1991a; Kern et al, 1991b; Pfister and Prives, 2017). This evidence concerns the gene TP53 and neoplasm.