Herein, TIMP-1 is shown to correlate with NOS2, pAkt, p-caspase-9, and nuclear pBAD in ER negative tumors (Table 2) and TIMP-1 suppression reduced NO-induced phosphorylation of PI3k/Akt as well as the downstream pro-apoptotic target BAD in MDA-MB-231 cells grown in culture, which further supports a role for this pathway in breast tumors. This evidence concerns the gene AKT1 and breast neoplasm.