Nonetheless, it is apparent that SAR1B contributes in a major way to hepatic lipid metabolism given the combination of our apoB lipoprotein studies (e.g.Figs. 1B and 2, D and E), the finding of hepatic steatosis in some children with CMRD (16, 17, 91), the highly significant positive correlations between SAR1B, APOB, and MTTP mRNA in human liver samples, and the finding that partial Sar1b knockdown reduced Srebp2 processing (Fig. 6H) paired with the expected corresponding reduction in levels of mRNAs encoding enzymes active in cholesterol biosynthesis (Fig. 4C). This evidence concerns the gene APOB and fatty liver disease.