While mutations that poorly activate LCAT associate with low apoA-I and HDL cholesterol levels due to the rapid removal of lipid-poor discoidal HDL from the circulation [30], mutations that cause amyloidosis may [5], [6] or may not [9]–[11] associate with low apoA-I and/or HDL cholesterol, most likely depending on the severity of the mutation [8]. The gene discussed is LCAT; the disease is amyloidosis.