A variety of medications work through AMPK and its downstream pathways. For instance, the biguanide drug metformin, in use since the 1950s, is a very effective agent for the treatment of type 2 diabetes, insulin resistant states, pre-diabetes, and cancer (Rojas and Gomes, 2013). Metformin acts primarily in the liver by reducing glucose output and, secondarily, by augmenting skeletal myocyte glucose uptake. Many mechanisms are involved in the beneficial effects of metformin on cellular metabolism; the activation of an upstream kinase, liver kinase B1 (LKB1), increased cellular AMP levels, and consequent AMPK activation are considered to be key mechanisms for the action of this drug (Zhou et al., 2001; Grahame Hardie, 2014).