Several genetic and epigenetic alterations that lead to genomic instability and loss of tumor suppressor genes (TP53, CDKN2A, RB1, RBL1/2) as well as activation of oncogenic signaling pathways including epithelial growth factor receptor (EGFR), phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK), and Janus kinase/signal transducers and activators of transcription (JAK/STAT) have been associated with oral cancer [9, 10]. The gene discussed is MTOR; the disease is lip and oral cavity carcinoma.