Previous studies have found that bilirubin impairs bactericidal activity of neutrophils through scavenging reactive oxygen species (ROS) and increasing NADPH oxidase-1 (NOX-1) and cyclooxygenase-2 (COX-2) in patients with hyperbilirubinemia, resulting in physiologic effects mitigated by increased antioxidant activity [12, 13]. This evidence concerns the gene PTGS2 and Hyperbilirubinemia.