This may be explained with the nature of CIN, which was caused by a failure in repairing DNA double strain break (DSB) due to the germline or somatic mutation of some genomic homeostatic genes, including homologous recombination repair (HRR) genes (e.g., BRCA1, BRCA2, PALB2, RAD51C, BRIP1) and genome caretaker genes such as TP53. Aberrant expression of TP53 disables cellular response to DNA damage on multiple levels [26]. This evidence concerns the gene RAD51C and cervical squamous intraepithelial neoplasia.