Mechanistic reports point to several nodes relevant to diabetes: activation of phosphoinositide 3-kinase (PI3K)/AKT [5], engagement of nuclear factor erythroid 2–related factor 2 (Nrf2) with possible AMP-activated protein kinase (AMPK) participation [6], attenuation of cyclooxygenase-2 (COX-2) with implications for arachidonic-acid-derived mediators [7], and promotion of glucose transporter 4 (GLUT4) trafficking in skeletal muscle [4]. This evidence concerns the gene PTGS2 and diabetes mellitus.