In a cervical cancer model, overexpression of the HPV oncoprotein E6 can maintain the stem-cell phenotype and stemness of CSCs through upregulation of Hes1, and short interfering RNA (siRNA) silencing of E6 or Hes1 leads to redifferentiation loss of self-renewability/stemness of CSCs [32]. Here, HES1 is linked to cervical carcinoma.