In the studies present in this report, increased expression of activated Akt-1 resulted in the resistance of MCF-7 breast cancer cells to both chemotherapeutic drugs (doxorubicin and etoposide) as well as hormonal based drugs (4HT) and these drug resistant activated Akt-1 overexpressing cells were also hypersensitive to rapamycin, which reduced the concentrations of doxorubicin, etoposide and 4HT required to reach the IC50s in these cells. The gene discussed is AKT1; the disease is breast cancer.