The inefficient immune response has a substantial role in the HPV persistence, as shown by several papers reporting altered gene expression with increase in pro-proliferative gene levels, such as CDKN2A, and low expression of genes related to a good immune response (NCAM1), leading to inhibition of pro-inflammatory molecular cascade in the surrounding stromal environment in CIN and early CC stages [11,12,13]. The gene discussed is CDKN2A; the disease is cervical squamous intraepithelial neoplasia.