Both experimental and clinical data indicate that amplified EGF receptor (EGFR) and Kirsten rat sarcoma (KRAS) mutations were found in approximately 50% of patients [8], and both oncogenic molecules further amplify downstream signaling such as signal transducer and activator of transcription 3 (STAT3) and mammalian target of rapamycin (mTOR), resulting in enhanced proliferation, metastasis, and stemness. This evidence concerns the gene MTOR and sarcoma.