Such dissociation between plasma concentrations of apoA-I and HDL-C seems especially surprising for the apoA-I[K107del] variant that is also associated with hereditary amyloidosis (13, 14), a disease characterized by enhanced proteolysis of mutated apoA-I and deposition of protein fragments as fibrils in vital organs that lead to removal of apoA-I from the circulation. The gene discussed is APOA1; the disease is hereditary amyloidosis.