Co-existence of both mutations has also been reported in endometrial cancer.8 PTEN inactivation leads to AKT phosphorylation and consequently activation of multiple downstream substrates including the mTOR proteins, caspases, cell cycle proteins and NF-κB to promote cell survival, metastasis and chemoresistance.9, 10 Activation of the PI3 kinase-AKT pathway represents one of the major mechanisms employed by cancer cells for cell survival, and by extension the pathway is often deregulated in cancer cells that are refractory to chemotherapy. The gene discussed is MTOR; the disease is cancer.