Analysis of the activation of apoptotic pathways shows that combined MEK/mTOR inhibition induces apoptosis more robustly and more persistently in PTEN-loss contexts, thereby partly explaining therapeutic synergism in this molecular context; however, we are currently investigating whether other growth inhibitory and/or cell death mechanisms (e.g. cell cycle inhibition, autophagy) also contribute to the observed tumor inhibitory synergism, particularly in vivo. The gene discussed is MTOR; the disease is neoplasm.