These latter classes of drugs activate the hepatic adenosine monophosphate-activated protein kinase (AMPK) [11,12,13], phosphatidylinositol 3-kinase (PI3K), and protein kinase B (PKB/Akt) [14,15,16], stimulate fatty acid oxidation in an AMPK- and peroxisome proliferator activated receptor-α (PPAR-α)-dependent manner, and inhibit the interference with c-Jun amino-terminal kinases (JNKs) and insulin action activated by inflammatory cytokines and free fatty acids [17,18], all of which are new targets and new ways of reducing blood sugar, obesity, and diabetes symptoms. The gene discussed is INS; the disease is diabetes mellitus.