First, as there is hepatic dysfunction, it is obvious that there is defective gene expression, which contributes to decreased PON1 in these patients.[1] It has been reported that there was significant decrease in PON1 activity in CCl4 induced liver cirrhosis secondary to increased free radical generation.[26] Second, as a consequence of an altered synthesis and/ or secretion of HDL-C, which may be due to impaired lecithin:cholesterol acyl transferase (LCAT) activity.[1] We have observed positive correlation between PON1 activity and HDL-C levels in patients with falciparum malaria and sepsis. This evidence concerns the gene LCAT and Sepsis.