This hypothesis is based on the fact that a concurrent ApoA-1 (same in CO and GSO) and ABCA1 expression prevents hepatic steatosis by stimulating a lower deposition of FA (as TAG) and TC, while suppressing FA synthesis by reducing 27-hydroxyesterol levels [59]; this effect plus a higher expression of RCT-involved enzymes/proteins in (SR-B1) and out (LCAT/HL) the liver may stimulate a more efficient FA and TC mobilization. This evidence concerns the gene ABCA1 and fatty liver disease.