We previously reported on a mouse model of VLCAD deficiency[1], [10], [23] that exhibited lipid accumulation in the heart as well as the marked induction of several indictors of lipid metabolism at birth, including PPARα, adipophilin and acyl-CoA synthase prior to any microscopic evidence of lipid droplets in the heart.[1] We performed cDNA microarrays of the VLCAD-deficient hearts[2], [3], [4], comparing one-day-old VLCAD-deficient hearts to wild-type controls. Here, PLIN2 is linked to very long chain acyl-CoA dehydrogenase deficiency.