Since SKP1 and CUL1 (i.e., SCF complex) normally regulate Cyclin E1 levels, we sought to gain mechanistic insight by determining whether aberrant Cyclin E1 turnover was responsible for the CIN phenotypes observed following SKP1 or CUL1 silencing. The gene discussed is CUL1; the disease is cervical squamous intraepithelial neoplasia.