The genomic instability that characterizes Pten-null cells may also originate from an aberrant activation of β-catenin, as β-catenin upregulation prevented the repair of recombination activating gene (RAG)-mediated DNA double-strand breaks in murine thymocytes, thus leading to Tcrα-δ/c-Myc translocations and T-cell lymphoma development [129] (Figure 2). This evidence concerns the gene PTEN and T-cell non-Hodgkin lymphoma.