Because activation of erbB2/erbB3 signaling resulted in paclitaxel resistance via PI-3 K/Akt-dependent upregulation of Survivin [27] and we showed that MM-121 mainly inactivated Akt in all three SKBR3 sublines (Figure 1B), we hypothesized that MM-121 might inhibit Survivin expression in both paclitaxel-sensitive and -resistant breast cancer cells. The gene discussed is AKT1; the disease is breast carcinoma.