Since the knockdown (or knockout) of different FATP isoforms reduces hepatic steatosis and in some cases increases insulin sensitivity and glucose handling, it is imperative that we understand the mechanism through which various FATP isoforms interact with different metabolic enzymes and/or intracellular transport proteins (L-FABP and ACBP) to regulate lipogenesis, TG synthesis and storage, and fatty acid oxidation pathways. This evidence concerns the gene INS and fatty liver disease.