As for Plaat3−/− mice, Sul’s group proposed that the reduced adiposity might rely on a decrease in PGE2, a PLA2-driven arachidonic acid metabolite, and thereby the reduced signaling of its receptor EP3 in WAT [83]; however, the causal relationship between the reduced PGE2-EP3 signaling and lipodystrophy is unclear since none of the knockout mice for PGE2 synthases or receptors displayed a similar phenotype. Here, PLAAT3 is linked to lipodystrophy.