In the first instance, we set out to model the HRD CIN class, using CRISPR/Cas9-mediated gene editing to first mutate TP53 then BRCA1, followed by overexpression of MYC. A panel of derivative subclones was subjected to functional assays, karyotyping and transcriptional profiling to determine (1) whether CIN had been induced and (2) what the potential mechanisms might be. The gene discussed is BRCA1; the disease is cervical squamous intraepithelial neoplasia.