CDKN2A and vulva cancer: Among the included studies, HPV-positive rate independent of p16INK4a ranges between 0% and 41% [23,25,27,34],which is in accordance with the fact that vulvar cancer presents an overall HPV infection rate of only 30%–40%[51–52].Moreover, the analysis outcome shows that p16ink4a overexpression correlates significantly with the HPV-positive status, strongly supporting the etiological role of HPV infection in the development of vulvar cancer.