AKT1 and breast carcinoma: Figure 10 demonstrates NO-induced phosphorylation of PI3k p85 at 60, 100, and 500 μM DETA/NO, which was diminished in TIMP-1 knockdown cells. Together these results suggest that TIMP-1 nitration may, at least in part, be an important event in NO-induced PI3k/Akt/BAD pro-survival signaling and that elevated TIMP-1/NOS2/pAkt may be useful predictors of breast cancer patient survival as summarized in Figure 11.