Statin inhibition of HMG-CoA reductase enzymatic activity in normal cells and statin-sensitive cancer cells [17] is known to activate a series of feedback responses, including modulation of AMPK, which in turn fine-tunes the levels and activity of HMGCR and Sterol regulatory element binding protein (SREBP)1 and SREBP2, leading to homeostatic levels of the cholesterol pathway [17–19]. This evidence concerns the gene HMGCR and cancer.