These studies indicate that the biological function of RASAL2 is influenced by cellular context to influence its pro or anti-oncogenic activity in human cancers [25] and different signaling pathways (as well as cross-talk) of RAS signaling pathway, the RAS-ERK pathway, phosphoinositide-3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) signaling pathway, and nuclear factor (NF)-κB pathway may account for the different biological outcomes of RASAL2 activity. The gene discussed is MTOR; the disease is cancer.