Those findings, coupled with the current observations in Mttp-IKO mice, suggest that the adaptive induction of Scd1 expression and function may mitigate the reversal of inflammatory signaling in the setting of established steatosis and fibrotic injury and further suggest that the overall distribution of FA species rather than simply the quantity of hepatic lipid is a key component of the injury phenotypes observed. This evidence concerns the gene MTTP and steatosis.