This raises the possibility that the tumorigenic activity we observed following expression of the Pik3caH1047R in immortalized cells may result from a cooperation between Pik3caH1047R and the dominant-negative p53 used for immortalization and provides further support for our contention that Pik3caH1047R alone is insufficient to cause cancer and that other secondary mutational events are required for tumorigenesis. Here, TP53 is linked to cancer.