This intravasation-promoting ability of Bcl-w was antagonized by expression of exogenous p53 or p53K305N, but not by p53R175H or p53K305N/R175H (Figure 8C), suggesting that nuclear and cytoplasmic p53 antagonize Bcl-w-induced tumor cell intravasation through transcriptional activity and Bcl-w binding, respectively. The gene discussed is TP53; the disease is neoplasm.