Heterozygous carriers of such variants (1:500 to 1:1,000 in Western populations) are often clinically asymptomatic, whereas individuals homozygous for APOB truncating mutations often exhibit very low LDL levels, fat malabsorption in the intestine, hepatic steatosis due to impaired VLDL secretion by the liver, and high prevalence of severe fibrosis (52–54). The gene discussed is APOB; the disease is fatty liver disease.