AMPK is activated by a wide range of stimuli, such as nutrient deprivation [4], cellular stresses [5], fasting or caloric restriction [6], caloric restriction mimetics [7,8,9,10], and nucleoside analogues such as (5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside; AICAR) [11], and has been evaluated in clinical trials for the treatment of metabolic diseases and cancers, including both hematopoietic malignancies and solid tumors [12,13,14,15]. The gene discussed is PRKAA1; the disease is cancer.