Surprisingly, even the most promising APC/CCdc20 inhibitor molecule apcin gave an unexpected result, namely, in the absence of mitotic poisons, it induced the expected cell cycle arrest at metaphase, but in the presence of mitotic poisons, which would be the expected conditions in cancer cells in individuals undergoing chemotherapy, apcin induced ‘mitotic slippage’, rather than preventing it, by not only decreasing APC/CCdc20 activity, but also by blocking mitotic checkpoint MCC function, the opposite of the desired result [24]. Here, APC is linked to cancer.