Similar to loss of p53 or overexpression of Mdm2, intraductal injection of lentiviral particles expressing Cre and C16orf72/HAPSTR1 or USP7 significantly reduced the latency of Pik3caH1047R-driven mammary tumor development, which was strictly dependent on the presence of p53 within those mice (Fig. 6E). This evidence concerns the gene TP53 and breast cancer.