Previous work by our group [9] and others [10–15] demonstrated that mutational activation of the phosphatidyl-inositol-3-kinase (PI3K) pathway through loss of PTEN (phosphatase and tensin homolog deleted on Chromosome 10) or activation of the serine/threonine kinase Akt sensitizes tumor cells to the antiproliferative activity of mTOR inhibitors in preclinical models. The gene discussed is AKT1; the disease is neoplasm.