The results of the reported studies overall sustain the idea that the condition of abnormally high levels of the AurkA/TPX2 complex leads to the hyperactivation of AurkA and exacerbates the defects induced by the overexpression of the single components, thus favouring chromosome segregation errors, aneuploidy, and CIN propagation that are functional features for both cell transformation and resistance occurrence. This evidence concerns the gene TPX2 and cervical squamous intraepithelial neoplasia.