CGI-58 was identified as the causative gene in the rare lipid storage disease Chanarin-Dorfman Syndrome [12], but despite its well-documented role as a cofactor for optimal ATGL-mediated lipolysis, the phenotype of the CGI-58-/- mutant mouse is not identical to the ATGL-/- mouse, suggesting that it fulfills other cellular functions that are likely independent of ATGL in mammals. This evidence concerns the gene PNPLA2 and Lipid storage disease.