In H-SIL cases, harboring hrHPV DNA and with increased expression of ki67 but without the block-like pattern of p16 expression, we can hypothesize further mechanisms of carcinogenesis, different from the more well-known mechanisms of HPV16 and HPV18, leading to p53 inactivation and Rb blocking, the last one determining overexpression of p16 [24,25]. The gene discussed is TP53; the disease is squamous cell intraepithelial neoplasia.