Interestingly, other Notch receptors could contribute to the crosstalk with major cancer stemness regulators such as the Hedgehog pathway, as it was demonstrated that the silencing of Notch2 or Notch target genes HES1 and HEY1 depleted the population of Notch/Hedgehog overexpressing tumor-initiating cells in a cell model of prostatic cancer with acquired resistance to docetaxel [493]. This evidence concerns the gene HEY1 and cancer.