In 2008, Fu et al. [94] reported that the anti-cancer agent etoposide, which causes double-strand breaks in DNA by inhibiting topoisomerase II [95], activated AMPK; other DNA-damaging agents used in cancer treatment, such as ionizing radiation [96], or the ribonuclease inhibitor hydroxurea [97] have also been reported to do the same. This evidence concerns the gene PRKAA2 and cancer.