In CIN tumors, TP53 mutations were common, as were amplifications of the RAS receptor tyrosine kinase pathway (VEGFA, EGFR, ERBB2, ERBB3, FGFR2, and c-Met) and cell cycle mediators (CCNE1, CCND1, and CDK6) [5]. This evidence concerns the gene CDK6 and cervical squamous intraepithelial neoplasia.