Furthermore, apoAI and ABCA1 displayed vital roles in processes of HDL biogenesis and early studies reported that loss-of-function mutations of these two genes could cause HDL deficiency [30], HT was likely to increase the level of HDL-C via inducing the expression of apoA-I and ABCA1 in hepatocytes, as seen by the results of Figures 3 and 5. The gene discussed is APOA1; the disease is hematocrit.