On the contrary, in group 2, including H-SIL cases with block-like p16 expression and increased Ki67 (3+), HPV 16 was the most frequent genotype (7/10 cases), in keeping with the hypothesis previously proposed that the oncogenic effects of HPV16 are strictly dependent on the inactivation of Rb, with consequent quick increase of p16 transcription, resulting in early block-like p16 over-expression [16]. Here, CDKN2A is linked to squamous cell intraepithelial neoplasia.