AKT1 and breast carcinoma: Although entinostat inhibited PI-3K/Akt signaling and activation of the PI-3K/Akt pathway led to Survivin upregulation in breast cancer cells [17, 19], it had no effect on phosphorylation of Akt (P-Akt) and MAPK (P-MAPK) in NSCLC cells (Figure 2C).