While determination of the precise lipid mediators involved remains a subject for future studies, it is intriguing to note that elevated levels of prostaglandin E2 (PGE2), a classic eicosanoid produced by the sequential action of cyclooxygenase and terminal prostaglandin E synthase on arachidonic acid, have been reported to contribute to defective differentiation of human myoblasts from myotonic dystrophy type 1 (DM1) patients with large CTG repeat expansions [35]. This evidence concerns the gene PTGES and myotonic dystrophy type 1.