The result we obtained on mTOR phosphorylation by rapamycin and LNC-rapa associated with of HIF-1α down regulation and Akt phosphorylation can be linked to the observation made by Hudson et al. who reported that rapamycin inhibits both stabilization of HIF-1α and the transcriptional activity of HIF-1 in hypoxic cancer cells and mTOR dependent signals stimulate HIF-1α accumulation and HIF-1 mediated transcription in cells exposed to hypoxia or hypoxia-mimetic agent (Zhong et al., 2000). This evidence concerns the gene AKT1 and cancer.