Consistent with an extrinsic mechanism of rapamycin resistance, our genomic survey of S2 tumor samples failed to identify significant copy-number alterations within genes in the mTOR pathway (FKBP12, S6 kinase 1, RAPTOR, RHEB, Akt) that might explain the observed rapamycin resistance in vivo. The gene discussed is AKT1; the disease is neoplasm.