The outcomes of the phase 1 clinical trial on patients with higher level solid tumors indicate that the mixed dosing seems to be well tolerated, at the least as well as single agent dosing. The combined effects of inhibiting MEK with Lapatinib price PD 0329501 and mTOR with rapamycin or its analog AP 23573 were examined in animal models of human lung cancer, in addition to in human NSCLC cell lines. PD 0325901 and rapamycin confirmed synergistic inhibition of proliferation and protein translation. Elimination of both MEK and mTOR inhibited ribosomal biogenesis and was connected with a stop inside the initiation stage of translation. The pan mTOR inhibitor AZD 8055 is examined as a single agent and in combination with the MEK inhibitor AZD 6244 in a NSCLC xenograft model. The combination resulted in enhanced cell death and tumor regression. These preclinical results support suppression of both the mTOR and MEK pathways in lung cancer treatment and indicate that both pathways converge to regulate the initiation of protein translation. ERK phosphorylates p90Rsk and Mnk1/2, which regulate the activity of the eukaryotic Urogenital pelvic malignancy translation initiation factor eIF4E. The phosphorylation of 4EBP1 is altered in cells with the BRAF mutation. It will also be remarked that the 4EBP1 is also regulated by mTOR, Akt and p70S6K. This may lead to the translation of specific mRNAs in BRAF mutant cells. This may describe how co inhibition of mTOR and MEK synergize to inhibit progress and protein translation in a few lung cancer cells. mTOR inhibitors have now been coupled with HSP90 inhibitors to overcome opposition to rapamycin. The consequences of combining the MEK inhibitor RDEA119 and rapamycin have already been evaluated in various cancers including pancreatic cancer. The effects ALK inhibitor of combined inhibition of IGF 1R and mTOR have now been analyzed in myeloma and other cancers. Also the effectiveness of combination of rapalogs and EGFR inhibitors to inhibit glioblastoma growth has been examined. The anti-proliferative effects of the Akt inhibitor perifosine is improved when coupled with nanoparticle bound rapamycin on multiple myeloma cells. Therapy of vemurafenib resistant BRAF mutant colorectal cancer cells using an Akt inhibitor overcame their opposition to vemurafenib. Heat shock inhibitors such as the HSP90 inhibitor XL888, have been proven to inhibit growth of some vemurafenibresistant cancer cells. XL888 increased proapoptotic Bim expression and decreased Mcl 1 expression. Also lowers in IGF 1R, COT, PDGFR beta, Raf 1, A Raf, S6, cyclin D1 and Akt were seen. This resulted in expression of the proapoptotic Bim protein and lead to nuclear accumulation of FOXO3a. Clinical Studies In relation to Inhibiting both Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Trails. Combinations of Raf and PI3K/mTOR or MEK and PI3K/mTOR inhibitors are in clinical trials.