A recent study by Chaurasia et al. using ablation of the enzyme dihydroceramides desaturase 1 (DES1) from whole animals or tissue-specific deletion in the liver and/or adipose tissue found that inhibition of DES1 resolved hepatic steatosis and insulin resistance in mice caused by leptin deficiency or obesogenic diets, enhanced activation of AKT/PKB in vivo, and elicited a broad spectrum of metabolic benefits characterized by improvements in glucose and lipid handling. This evidence concerns the gene AKT1 and fatty liver disease.