Numerous studies suggest that the pathophysiology of CIN/ICUS-N is attributable to apoptosis of developing neutrophils in the bone marrow mediated through activated T lymphocytes and excessive production of pro-inflammatory and myelosuppressive cytokines such as IFNγ, TNFα, and Fas-ligand [46,47,48,49]. The gene discussed is TNF; the disease is cervical squamous intraepithelial neoplasia.