This relative enrichment of VLDL during hypertriglyceridemia has been proposed to result from 1) increased hepatic apoC1 production coupled with enhanced VLDL secretion and/or 2) redistribution from HDL to VLDL in the circulation [3] since apoC1 has been demonstrated to be a highly exchangeable protein [4, 40]. The gene discussed is APOC1; the disease is hypertriglyceridemia.