Gene mutations (e.g., PIK3CA, PTEN, and RICTOR) and activation of the PI3K/AKT/mTOR have been reported in genomic and proteomic profiling studies of SCLC tumor samples; however, there have been notable discrepancies in the results, due perhaps to relatively small sample sizes, differences in population (e.g., race, naïve or chemo-resistant) and sequencing techniques [8, 10, 12, 41]. The gene discussed is AKT1; the disease is neoplasm.