Human data do not support an increased prevalence of hepatic steatosis in ANGPTL3-deficient subjects [15,33] suggesting that fluctuations in the availability of substrates, plasma glucose and insulin concentrations in vivo as well as uptake of glucose and fatty acids by other tissues regulate hepatic glucose uptake and VLDL secretion and thereby preventing hepatic TAG accumulation in ANGPTL3-deficient individuals. This evidence concerns the gene INS and fatty liver disease.