There are several possible explanations for this cancer-selective phenomenon: (i) nonmalignant cells have the ability to regulate Myc expression and respond to elevated levels of Myc76; (ii) the cells lack cancer-driving properties, such as unregulated proliferation, oncogenic activation of Myc, and most importantly, chromosomal instability77,78; and finally, (iii) an additional checkpoint exists at the end of G2, prior to mitotic commitment, that is independent of the DNA Damage Checkpoint. This evidence concerns the gene MYC and cancer.