For example, compensatory activation of MEK and/or AKT has been shown to limit mTOR/PI3K inhibitor therapy in prostate and breast cancer cell lines and patient tumor samples, which could be reversed by combined inhibition of mTOR/PI3K and AKT (Carracedo et al. 2008; O’Reilly et al. 2006). The gene discussed is AKT1; the disease is neoplasm.