This high frequency of the premature termination/truncation of translation is strongly analogous to “four well-established tumor suppressors (PTEN, TP53, FBXW7, and CDKN2A), and PPP2R1A, a central component of the protein phosphatase 2A (PP2A) complex that also functions as a tumor suppressor” [30], regardless of the difference in the mutation spectrum. This evidence concerns the gene PTEN and neoplasm.