Consistent with these observations of a tumor suppressive function of IFIT2, its depletion in OSCC cells induced EMT and cancer stem cell-like phenotypes, enhanced cell migration and invasion and metastatic activity via mechanisms that potentially involve mediation of atypical PKC (Protein kinase C) signaling and TNF-alpha upregulation [58,59,60,61]. The gene discussed is IFIT2; the disease is neoplasm.