On the other hand, decreased amounts of I-FABP are observed in patients with ABL and CRD in link with the pathological intracellular accumulation of lipid structures in the enterocytes, leading the investigators to hypothesize that I-FABP acts as a lipid sensor to prevent the intracellular esterification of FA into TGs which would otherwise lead to further additional intestinal injury (Guilmeau et al., 2007). The gene discussed is FABP2; the disease is abetalipoproteinemia.