Nevertheless, from a narrative synthesis point of view, three of the studies included in this systematic review have shown that tissues with high expression of SP/NK-1R also showed Ki-67 overexpression in oral squamous cell carcinomas, oral lichen planus, and keratocystic odontogenic [11,28,47]; therefore, uncontrolled cell proliferation could be the putative oncogenic role of SP/NK-1R in pre-malignant and malignant cells, potentially activating downstream central oncogenic signaling pathways (i.e., MAPK and PI3K [15,16,17,18,19]). Here, MKI67 is linked to oral lichen planus.