While the full extent of PCP4/PEP19 involvement in inhibiting the apoptosis signaling pathway in breast cancer cells is still to be elucidated, we hypothesized that PCP4/PEP19 expression in ER-negative SK-BR-3 cells may be a contributor to estrogen hypersensitivity that results from estrogen-deprivation resistance, through cross-talk with multiple signaling pathways, such as the mitogen-activated protein kinase (MAPK) and Akt [39-41]. Here, AKT1 is linked to breast carcinoma.