Despite the similar lipodystrophy phenotype in Prmt5AKO and Bscl2AKO mice, the hepatic steatosis, insulin resistance, and lowever energy expenditure of Prmt5AKO mice were not observed in Bscl2AKO mice.[25] The distinct phenotype may be explained by additional targets of PRMT5 besides Seipin. This evidence concerns the gene PRMT5 and steatosis.