Drugs that inhibit targets broadly associated with CIN, such as polo-like kinases, cyclin-dependent kinases, and Aurora kinases are being explored in clinical trials, and histone deacetylases (HDAC1, HDAC5, and SIRT1) are being evaluated for efficacy in inhibiting centrosome duplication and amplification [61, 64–66]. Here, HDAC1 is linked to cervical squamous intraepithelial neoplasia.