Carcinogen exposure can trigger a complex multistep process characterized by an accumulation of 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) that contribute to oral cancer progression [9,10]. Here, MTOR is linked to lip and oral cavity carcinoma.