Though the exact cellular and molecular mechanisms of β-cells causing pathogenesis of diabetes mellitus are still under investigation, certain therapeutic targets in β-cell for the bioactive compounds have already identified such as nuclear receptors (e.g., peroxisome proliferator-activated receptors (PPARs)), cell membrane receptors (e.g., K+/ATP channels, Na+/Ca2+ exchanger, GLP-1R), transcription factors (e.g., PDX1, Ngn3), and intracellular enzymes (e.g., glucokinase) [140, 141]. The gene discussed is GCK; the disease is diabetes mellitus.