However, this set of phenotypes would strongly reinforce the hypothesis that targeting the interactions between Apc1 and/or Apc5 and the Cdc20 protein in this specific loop regions does have promising potential, because they would satisfy the first and third criteria stated above: that the mechanism of action of the small molecule only causes an extended mitotic arrest in the presence of a mitotic poison to prevent cancer cell ‘mitotic slippage’, and that it specifically inhibits APC/CCdc20 and not APCCdh1. This evidence concerns the gene ANAPC5 and cancer.