CLOCK and cancer: The competitive antagonism of the overexpressed stemness/reprogramming master factor dimer MYC/MAX with CLOCK/BMAL1, which is the core component of the CC’s activation arm and a regulator of the G2M DNA damage checkpoint, is likely to play a key role in impairing the CC in stem cells (including stressed cancer cells that have undergone reprogramming), where stemness features were shown to be tightly coupled to deregulation of the cell that leads to polyploidy.