Inactivation of POT1a in a p53-null context exacerbated the initiation of malignancy in mice; consistently, POT1 mutations were shown to cause predispositon to several types of malignant tumors, including cutaneous malignant melanoma, chronic lymphocytic leukemia (CLL), glioma and cardiac angiosarcoma [13–18]. This evidence concerns the gene TP53 and B-cell chronic lymphocytic leukemia.